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KB. v'l'.'.OM IV K II fiV ITOI I I; III PHCii;\j:. > IN hay,. a:.. i !; II. C. II > , I. A. I .yii I-.I. Jr. i;:ii. H1','. i' n, ,,. . :i .. it. .1. in .1.. ii <i ..) 'K!i;.vjor tee r.psms i:.vi by va>.- * 1CW PUSTJCl..E:iA, (timidity M.u.l;-n) G. Dortraunn ct el. Z. L'r.nKNSMiVv-'INTr.nSJJli 103, |-. '113 (1956) i:i:> 1 : -iv/ii:ity .vr"'.''i.; on two n01:idj .'iiYi.lJ.i; III-', III T':.. FAT AND P(,;i. p. A, l.il.ic/ii ' I- .1. TO* I *`>'i tc Alii.. I iiA IlM.ACOi 0.17 2, No. (1, p. V.J (November, I960) THE ACUTE TOXICITY OF THE THlAHYI. FHCSlTi.'Tc USED AS PLASTICl/.tKS. H. F. Bondy ct al. UNIT. .1. IN!). KKD. 1_7, | . 1 10 (3 9CO) y PROPOSALS FUH EVALUATION OF .Ti l.l i.KTJ C KATE.ilALE USED It. THE POOL INDUSTHY. (lovntiricatlon of plasticleers end atabi liters for packaging film!), and evaluation.-, of their' toxicity) n. Staub. mitt. mu.;.:;:., hyg, ^ p. l (19DB) V TKfc TOXICITY OF PLASTICS KATEnlALS. 2ACKA01NC Al, No. 3AZ, p, 72 (December 1958) j TOXICITY EXAMINATION CF PVC FOILS. 0. r Berndt. FLA5TE u. KAUT. 6, llo. 7. p. 3A7 (July 1959) INVESTIGATIONS OF THE TOXICITY OF POLYVINYL CHLOHIDE STABILIZERS, i. V.. Ncbel Sc O.R. Klimmer. AKZKE1K1TTEL-F0R5CHUNG 10, No. 1, p. 4A (January 1&60) THE TOXICITY OF PLASTICS, (especially lead ^ atabllliers) S. F.-Chancellor. NATURE 185, No. A716, p. 8A1 .(March 19, i960) PHYSIOLOGICAL AND TOXICOLOGICAL PROPERTIES, (Toxicity of vinyl resin stabilisers) R. Lefoux. PLASTIC.`JES INFORMATIONS 12, No. 257, p. A (1961) i SANITARY-CHEMICAL STUDY OF PVC-COATED FADi.j I N. 1, Slcpek. UCH. SAP. ROSE. IJAUCH. ISSL!-.. 1KST. GIGIENY, Ho. 9. p. 121 (1961) V THE TOXICITY OF RIOID PVC DRINKING WATER CC: ' DUITS, A. Hodayna. REV. BELGE KAT. FLASTI- QUES No. 1, p. 17 (January 1962) . TOXIC AND HEALTH EFFECTS OF PLASTICS AND P" RESINS. J. A. Zapr. ARCHIVES ENVIRONMENT, HEALTH A_, p. 335 (March, 1962) < A KINIF.UK STANDARD TO MAKE PLASTICS SAFE IN r MEDICAL APPLICATIONS. Dr. John Autlen. PLASTICS WORLD 20, No. 3. P- 12 (March, 1962) y .PLASTICS. (Review of toxicity references) R. H. Wilson tc W. E. McCormick. ARCH. IND. HEALTH 81, No. 6, p. 536 (I960) HEALTH AND SAFETY IN THE PLASTICS INDUSTRY. D. Kenwln Harris. PLASTICS INST. TRANS. 3C, No, 86 (April 1962) THE TOXICOLOGICAL PR0DIHS OF PLASTICS USED f- IN FOOD PACKAGING. IND. FLASTICUES MOD. 12, p. 69 (June i960) THE PROBLEM OF NON-TOXICITY CF ADDITIVES IN THE DOMAIN OF PLASTICS. E. LeClerc. IND. FLASTIQUE5 MOD. 1A, NO. 10, p. 37 (L^i. 1962' 48. VISCOSITY & FLOW PROPERTIES MEASUREMENT OF THE FLOW TEMPERATURE OF THER MOPLASTIC MOLDING MATERIALS. L. W. A. Meyer. A.S.T.K. BULL. No. 105, F. 23 (August, 19AC) FLOW TEMPERATURE OF THERMOPLASTICS. L. W. A. Meyer. MOD. PLASTICS 18, No. A, p, 59 (December 19A0) FLOW PHOFEHTIES OK THERMOPLASTICS. 1. W. G. Wearmcuth tc J. S. Small. BRITISH PLASTICS 12, No. 1AA, p. 377 (Kay ls'll) WORKING-RANGE FLOW FRCFEHTIES of THERMO PLASTICS. F. E. Wiley. I NT). E'.'G. CHEN. ^3, No. 11, p. 1377 (November, IS'll) SOKE RHEOLOGICAL PROPERTIES OF rOLYVINYL CHLORIDE. L. Bllmes, J. SOC. CHZM. IND. 63, No. 6, p. 1E2 (Juno I9AA) HIGH TEMPERATURE, HIGH PRESSURE RHF.CF.ETEH FOR PLASTICS. H. K. Nason. J. APPLIED PFTS. 16, Na. 6, p. 338 (June 19*15) RHEOLOGICAL i'LORI.r."..', IN THE PIIOC.ESNIHC CM PLASTICS, ii. BuehJahl Sc h. K. Ns;.on, IND. ENG. CHEN. AO, No. A, p. 6A2 (April ISAS) VISCOELASTIC fr-'IEPTIF: 7-:;. --T.7. P LLYME.iS. K. Hsrlo et ai. J. APPLIED PHYS. 22, No. 7. p. 966 (July 1951) RHEOLOGY AND THERMOPLASTICS. E. E. Atkinson t K, A. Nancarrow. PLASTICS l:;ST. TF.ANS. J54 11, No. 38, p. 23 (October, 1951) APPLICATION OF NUTTING'S EQUATION TO VISCO ELASTIC BEHAVIOR OF CERTAIN POLYMERIC SYSTEM R. Buchdahl tc L. E. Nielsen. J. APPLIED PHYSICS 22, No. 11, p. 13AA (November, 195-1 THE ELASTIC-VISCOUS BEHAVIOR OF PLASTICIZED POLYVINYL CHLOHIDE AT ELEVATED TEMPERATURE. W. Tsujl 4 K, Shlosawa. BULL. INST. CHEK. RESEARCH, KYOTO UNIV. 27, p. 67 (1951) TWO EXTRUSION PLASTOKETERS FOR USE WITH POLY VINYL CHLORIDE. R. Hayes. PLASTICS 17, No. 177, p. 10A (April 1952); and CHEK. & IND. .(1952) p. A21 and p. 1069 VISCO-ELASTICITY OF HIGH POLYMERS. II. KINV, . BEHAVIOR OM PLASTICIZED POLYVINYL CHLORIDE NP;AR THE TRANSITION POINT, S. Nohnra tc S. Ouchl. CHEF, HIGii POLYMERS (Japan) 1C, p. 266 (1553) rOLYVINYL CBIXRIDP hEUN. IV, VISCOMETRIC STUDIES OF MAST!CAT..' l'VC, X. Goto rt al. CHEK. HIGH POLYMERS (Japan) 11., p. A37 (19p A KINETIC INTERPRETATION OF TEE RHEOLOGICAL ERRATIC" CF HIGH PoLYMERS. Jur,Ji .-uru,:awa . J. POLYMER SCI. 15, No. 79, p. 193 (Jenuar. 1555) INTERPRETATION OF BROOKFIELD VISCOSITIES. F.. L. Bowles, R. F. Davie tc W. D, Toad. MOD. PLASTICS ^3, NO. 3, P. 1^*0 (November, 1955) OIiI 5791 I.. I.IMw IIJM. X', CHEK. ACE 19, 1957) VINYL tllLOC. A. Kumlns 10, p. 1290 ILMS. V. E. N PLASTICS ^6, .ns TO 90% ietriek and SR SCI. 2, No. 1959) ,SU0P.PONR.TED . APPLIED (September/ IN CONTACT . Woelk. 5 (December TO CASES, B. 0 KAQAKU 5 POLYMERS TO rlln and K. p. 2252 >1- Ml kl-U, |. 1 17 (K'lilllity , J "I) on Tin. w,vm: vaiiih Ai- '! 1 in1: < :: 1-11,1:; I OWIH.1I1Foill'.LTJiT.; `Ml -11 I '-! II::..- n.oc'i'iNi dy so::;: iacka-.j:. ; >11. t. Makino ct al. KOCVC KAS/K'J LASS HI M, No. 7, P. 1255 (July 1961) THE PEW'.WiHILITY OF FVC-CELLULOSZ 1 AMINAT.-.', TOWARDS HYDROGEN SULFIDE AND AMMONIA. h. Braun!h and K. Lenhart, K0LL0ID-2E1T3 177. No. 1, p. 2A (July 1961) . PERMEABILITY OF FUSTICS. 1. Phillips and D. V. Bartlett. BRITISH PLASTICS No. 10, p. 533 (October, 1961) DIFFUSION OF GASES AND VAPCR5 THROUGH POLYVINYL CHLORIDE- POLYVINYL ACETATE COPOLYMER FILMS. I. GU5S TRANSITION EFFECT. II, THE EFFECT OF POLYMER SEGMENT MOBILITY. C. A. Kumlns end J. Rotcman. J. POLYMER SCI. jj. No. 162, p. 683 (December 1961) WVT THROUGH MULTIPLE BARRIERS. K. V. Nlnnemann and L. E. Slmerl. MODERN PACKAGING 25, No. A, p. 137 (December 196I) PERMEABILITY OF PLASTIC MATERIALS TO WATER VAPOR. Marie Korte-Fallnakl. J. CHIK. PHYS. 59, No, 1, p. 27 (January 1962) DIFFUSION OF GASES AND VAPORS THROUGH UN- FIOMENTED VINYL FILMS -- GLASS TRANSITION EFFECT. C, A, Kumlns & D. J. waythomas. OFF. DIG. J, TAINT TECH. <c ENG. No. AA5, I . I IV (Mlirinry ) ihr) m, in-:. 11 i.r. .. -n.itv Hi' iiiuii i"j.,v,.1. .'.ini'.,, rlA.iv u, MIFF, 1.11. 3, p. 117 (iN'iI-ch 196l) ACTION OF Lf,*-:;M,t;cUIJ.I, l.lflllDS 01. CERTAIN POI.YMHUC MATi.HIAIS. (HTcct-j Of limei.-ralnn In enter nnd t/aoUne) V. A. VoakrenonnKll. ZHUK. PKIKLAD KJilM. ?I5, Wo- 3' P. e'*G (1962); and J. ArpL. CKEK. 'J.S.S.R. 22' Ko- 3.- P* b70 DETERMINATION OF THE PERMEABILITY OK FUSTIC CONTAINERS TO OXYGEN. A. Douaa and V. Slmak. ODALY 6. No. A, p. 10A (1962) CAS PERMEABILITY OP FUSTICS. Coleman J. Major and Karl Kammermcyer. MODERN PUSTICS 29, No. 11. p. 135 (July 1962) HYGROrilOTOORAIHIC STUDIES ON THE PERMEABILITY TO WATER AND MOISTURE OP PACKAGING MATERIALS. J. Slvadjian and F. Corral, J. APPL. POLYMER SCI. 6, No. 23, p. $61 (September 1962) ISOSTATIC-CHEMICAL ANALYSIS METHOD TESTS FILM'S GAS PERMEABILITY. R. G. Marlett. PACKAGE ENG. 7, No. 10, p. 60 (October 1962) WATER VAPOR TRANSMISSION THROUGH POROUS FILMS. D. Setaa and D. C. Carr. J. APPLIED POLYMER SCI. 6, No. 2A, p. s-6A (November/becember 1962)" GAS CIIKOMATOOHAPH MEASURES FILM PERMEABILITY. H. L. Frickc. PACKAGE ENG. J, No. 12, p. 51 (December, 1962) jH POLYMERIC "-t and R. H, 51. 1. No. 7, 47. TOXICITY Af Sec topic 38, Packaging, for general references dealing with *toxici(j, problems. LMS FOR OASES THE DEGREE OF -"ION ON THE NSHI KAQAKU YMERS. H. H. POLYMER SCI. 3) D PVC, H. ). 12, No. 7, AD PVC. H. 5. P- 359 TIC FILMS, uary 1961) : LABILITY C . VI. TILE . Myere et nuary, 1961) HRS ON THE " .OUCH HIGH KAGAKJ ry, 1961) OF W. A. SKIN TROUBLES FROM TEXTILES. W. Schweis- helmer. TEXTILE COLORIST 66. p. 69 (Feb. I9AA) /'ACUTE AND SUBACUTE TOXICITY OF DI (2-ETHYL' HEXYL) PHTHAUTZ -- ITS METABOLISM. C. B. Shaffer et al. J. INDUS. HYG. k TOX. 27. No. 5, (May I9A5) HEALTH HAZARDS FOR PVC AND ACRYLICS? PUS/ TICS 12, No. 129, p. 65 (February I9AB) / TOXICITY OF O-TRICRESYL PHOSPHATE. 0. j ' Blomqvlst. SVENSKA FUST. FOR TEK. MED. 5, No. 1 (1950) I ^ THE TOXICITY OF TRICRESYL PHOSPHATE. N. j k Nelson. MED. BULL. NEW JERSEY 10, p. 11A I (April 1950) / STUDIES ON THE TOXICITY AND SKIN EFFECTS OF COMPOUNDS USED IN THE RUBBER AND FUSTICS INDUSTRIES, II. PLASTICIZERS, F. S. Mallctte k E. Von Haam. AHCN. INDUS. HYG. k OCCUP. MED. 6, No. 3, p. 231 (September, 1952) T0XICITIE5 0? BUTYL STEARATE, DI3UTYL / sf.ucatz, diuutyl PH',::;.: ;..... : u.-uAYETi.YL OLS/.TE. C. C. SmiU;, AF.Jil. IN-Jj:. HYG. k OCCUP. MED. 7, p, 310 (April, 1953) TOXICITY OF 2-ETHYLHEXYL DIPHENYL PHOSPHATE. / I. IMMEDIATE TOXICITY AND EFFECTS OF LONG TERM FEEDING EXPERIMENTS. J. F. Troon, F. R. Deutra k P. F. Cleveland. ARCH. IND, HYG. OCCUPATIONAL MED. 6, p. 170 (August, 1953) TOXICITY OF 2-ETHYLHEXYL DIPHENYL PHOSPHATE. III. STUDIES OF THE EXTRACTION OF SANTICIZER lAl FROM POLYVINYL CHLORIDE FILMS BY FOOD STUFFS UNDER VARIOUS CONDITIONS OF STORAGE. J. Clark Kaakle, ARCH. IND. HYG. OCCUPATION AL MED. B, p. 281 (1953) OCCUPATIONAL DISEASE IN THE MANUFACTURE OF POLYVINYL CHLORIDE PRODUCTS, (when contain ing chlorinated naphthalene) J. Roubal k F. Pokorny. FRACOVNI LEKARSTVI 5, p. 1AA (1953) / TOXICOLOGY OK PUSTICS AND RUBBER -- PUSTOMERS AND MONOMERS. Rex R, Wilson k Wm. E. McCormick. IND. MED. k S'JHGERY 23, p. A79 (November, I95I;) y FURTHER STUDIES OF POLYMERS AS CARCINOGENIC AGENTS IN ANIMALS. B. S. Oppenheimer et al. CANCER RESEARCH 1, P. 333 (1955) SOI": ASPECTS CP THE TOXICOLOGY OF FUSTICS, H. Korquct. KAl'ERIE PLA5T1CHE 22, NO. 2, p. 100 (February 1'956) X v CHRONIC ORAL TOXICITY OF 2-ETHYL HEXYL OLI 5792 523 C9le 3 Clienm.d /ilv.li.icl4. Vol /J, I'M.') l .i- /.(. wax nibed with iltftlillin 11 Itt'in (0." ml.) and iiieol, ,1, d with antihi.m at 37* lor Ii ifiiv, in medium l!l*i. "I In- mm. ('>mm COUCH. ill'll), by l)i>' llirl.limin' fill-*ftltfi*ill*1 te-.l tc.iilil |ln mil ml Urns 1U'* JU"` M/ml. Tin' ii -.1 wax iipplied n inr. <.>m`i- <>( in oculum si/.is, vok,, lll-l), rniini. anil iitililnxiii omen. Vari ance v.a* nonpareil wit Ii V',;. in tin* fy 1 opii h- n-itn'ii y but the method was easier ami was suitable (nr M'lial bdu. up. plication. Teter M. Motion 59]05g Toxicological investigation of cyanides. Orlira, Manuel; Vulfi in, K. (Inst. Nac. Toxicol., Madrid, Spain). An. Real Awl. Pin in. I960, 32(4 5), -I"!! HI (Span). lllood (1-0 ml.) or mimed viscera (2-3 g.) was plarnl in a Cornvny cell for 4 lirs. willi 1-3 drops of 107?, 1ESO, ami HCN evolved was absorbed in 0.1 A' NnOli. To the latter were added 2 mi. M Na* HifOi and 1 ml. 0.25% chloraminc-T, then after 2-3 min., 3 ml. reagent (3 g. barbituric ncid, 16 ml. pyridine, 3 ml. HCl, and water to 50 ml.). The red to reddish purple Color was read at 5S0 mft after 10 min. Ilccr's law was obeyed for (1.5-2 y KCN/ml. With time, cadaver C,N" is converted to CAS-, To dot. this, blood or viy-cru was deproH-imzed by adding an Cf|Uat amt.of III- PO,, heating to boiling for 10 min., and adding 50 mg. of powd. picric acid/g. of tissue. After 12-2-1 hrs, at room temp., it was filtered and 1 /3 vol. 5% KjCrjOi and 2/3 vol. 50% HiSOt were added to the filtrate in a Conway cell. l>etn. of CM' was as above. Recovery of added CA'S* was 51 % (7% if not depro* teinited). Disopprarar.ee of CN postmortem is approx, ex potential and the amt. present at death cannot be accurately ealed. from subsequent detns. J. R. Gwilt 59l06h Identification of hashish (Cannabis estiva), Cham- bon, Paul (Fac. Med. Pharm. Lyon, Lyons, Fr,). Bull. Trav. Sot. Pharm. Lyon 1068, 12(1), 43-0 (Fr). A sample o( hashish was identified using color reactions and thin-layer ehromatog. On silica g>i f`>. The principal constituents were cannabinol, Cannabidioi, and tetrahydrocannabinol. Dorothy J. Buebanan-Davidson S0107j Identification and determination of nonvolatile or ganic poisons by infrared spectroscopy in forensie toxicology. Cor- neteau, H.; Monnet, R.; Boitcau, H, L. (Fac. Mist* Med. rhasm. Nantes, Nantes, Fr.). Med. Leg, Vomm. Corpor. 1668, 1(4), 352-9 (Fr). Eleven alkaloids and 0 neuroleptic agents were identified and cstd. by ir spectrometry after exin. and sepn. by thin-layer ehromatog. on silica gel. The chromatogram elu- ates were coned, on KBr micropcllets. Spots contg. 10 y of eompd. could be estd. with a precision of 6-15%. L. A. Dehennin 59108k Utilization of an anti-y-globulin immune serum for determining the human origin of blood stains. Tran Van Ky, Philippe; Lenoir, L.; Muller, P. (Inst. Med. Legale Lille, Lille, Fr.). Med. Leg. Vomm. Corpor. 1968, 1(4), 392-5 (Fr). Extn. of a blood spot with isotonic phosphate buffer of pH 7.4 exts. the antigen. Monospecific antisera are obtained from rab bits immuniied with human *>G-globulins. The immunologic tests are performed by double diffusion on gclose. L. A. Dehennin 59109m Evaluation of postmortem blood eugar levels and their correlation with the glycogen content of the liver. Ramu, M.; Robinson, Ann E.; Camps, F. E. Med. Set. Loro 1969, 9, 23-6 (Eng). Satisfactory blood glucose estns. may be made by using blood samples collected into tubes contg. F~ up to 48 hrs. after death, provided that a specific assay procedure is used. The blood glucose concn. for samples from the left side of the heart and the upper and lower extremities statistically belong to 1 group whereas the right heart blood and the liver blood belong, statistically, to 2 different groups. There were no significant variations in the blood glucose concn. with the time interval 12- 48 hrs. after death. There is a significant inverse relation be tween liver blood glucose conens. and the glycogen content of the liver asassayed ehem. irvmg Sunshine 59110c Relations between the levels of alcohol in the blood and in the breath. I'anlucci, 0. Riv. Med. .Irmnaut. .Spue. 1968, 31(3-4), 4U1-0 <Itai), 'lots wore made with 2d subjects (2 female) of av. age 35 who consumed, in a single dose, I).fill g, EtOH/kg. in the form of cognac. Exhaled air was collected every 15 min. tip to 2 hrs. after ingestion and blood v.as sampled at 45 and 120 mm. in 15 of the subjects and every 15 min. in the remaining 6. To del. whether differences existed between the air exhaled in 1 profound expiration and alveolar air, the latter was collected in equal vol. immediately after the former. The blood EtOir increased regularly lip to 60 min., then decreased irrer`j!..r!;` no t x 2 hrs Tb- .-a4,* 4 E4* |li m 34 44> in' evb.d-d air to that m 1 mi. biood was ab>*ui i .2 lor th- iir. u.'.< i n.- Jtmion, varying with the individual . IE,aid i'4.(4:i is detectable up to 2 hrs. i'i subjects with considerable adipose ti-suc but lias practically disappeared after 1 hr. m lean subjects. J. I. M. Jones 591 Ilf Fractionation analysis of metallic poisons. Krylova, A. N. Vofir. Sudebnot Mid., Mtn.Zhravookhr. SSSIi 1968, 314- Si (Russ). From Ref. Zh., Kilim. 1969, Abstr. No. 2G175. A e imr>iriso4i of the accepted H;S method and the new fractioua. -- ...... a,..;-, . -- 1 o--.c c- jc made. with itiiiiofi to a group of 12 iHiisotis (l4b, It.i, A-., Ah, lli, II,4, (n, I'd. Ag, /n. I'i, :ol Mn l. On.il. mid ipinnl. mini, inei|,.,,U tali I 2 wmLmg day. m li-ml of lb*- K frapihul bn ill' ll S m-'thiid, with eir.ilri ci-ucitivily mid iimitiii'y, MOIM. Sol Up Si-piuiilnm of nipper and i ndmiiim by extraction in (nrcm.ii chemical investigatimii, Kiytov.i, A, N. Vufit. Sml.-I. nut V/ih. Z.linr.^Hiblir. .V.X'.SA4 I*1011, 32*3 7 (Itnxs), i-ioin A'ct. Zh., Lhim, 1969, Ale lr. No, 2GIVti. A im-tlmd of extn. and eomph xomctric clctn. of Cu and Cil in human organs is ib- sctiled Mineralise the sample with }INOj-HiSOt, add 20 ml. 2d' i V. Na tartrate, 10 ml. glycerol (1:10), and 30% KOIt until in-pn >1 mid ft nil. in exrexs. Add 10 ml. 171 Na dietliyldithio- raili.iiu.iv (l)tiiid 111 15 ml. CIlCIi, shake, and re|H4:it tin-<\ln. until a cnlorltss CllCli layer is obtained. Keext. Cd from the comlnmil ext. by shaking with 10 ml. N I1C1 (3 times). Dil. the Cd cm. to 100 ml. with lljO and bring to pll 8. Titrate Cd with 0.01 ,Y EDTA until the red-violet color changes to dark blue. Wash the CllCb ext. 3 times with 10 ml. 5N HCl (to remove Bi am! 'J i/ ami then with HrO until neutral reaction. Ext. Cu by shaking with 17?. llgClt until colorless, and dct. in the ext. ky turn, with EDTA in the presence of murexideand 1-2 g. K1 at pll K (color change from yellow to violet). MQUK 59113b Biochemical modifications induced by acute and sub acute intoxication with white phosphorus in the rat. I. Action of repeated parenteral doses. Truhaut, Rene; Claude, Jean K.; Warnet, Jean M. (Fac. Pharm., Paris, Fr.). Ann. Pharm. Fr. 1969, 27(1), 17-23 (Fr). Repeated administration o( white P to rats, parcnterally, decreased body wt. A dose of 2.5 mg./kg. de creased liver wt. without visible steatosis; liver triglycerides were increased and - phospholipids decreased, leaving the total lipid content nearly const. In the blood both total lipids and tri glycerides were lowered. With 5 mg./kg. several rats died after 7-8 days following the 3rd injection, and all showed varying de grees of liver steatosis with increase in triglycerides and in total lipids. Since the activity of glucosc-O-phosphate dehydrogenase remained normal it is unlikely that the biosynthesis of fatty acids and triglycerides was increased, Ruth At, Chester 59114j Toxicity of pyrolysis products of vinyl plastics. Corn- ish, Herbert H.; Abar, Ellen L. (Sch. of Tublic Health, Ann Arbor, Mich.). .1 rch. Environ, flrallh 1969, 19(1), 15-21 (Eng), Poly(vinyl chloride) (1) and vinyl chloride-viny! acetate poly mers (II) were pyrolyxed in air by gradually raising the air temp, from ambient to COO*. Rats were exposed to the pyrolysis prod ucts air stream dild. with room air to twice its initial vol. Ex posure to air contg. the pyrolyicd products from 1-2 g. 1 resulted in death to 50% of the animals. Most deaths were due to CO, and carboxyhcmoglobiuTcvcls correlated well with the amt. of pyrolyzed I. Little histol. evidence of lung damage was evident. When the air stream was dild. with O, pulmonary edema and in terstitial hemorrhage developed. The lungs of animals exposed to high levels of II pyrolysis products showed focal edema and intraalveolar hemorrhage, I formulations contg. additives and inert materials were generally less toxic per g. of sample pyro- lyicd. BZJN 59115k Validity of a critical blood level for prevention of di- eldrinintoxication. Keane, William T., Jr.; Zavon, Mitchell R. (Agr. Chem. Div., Shell Client. Co,, New York, N.Y.). Arch. Environ. Health 1969, 19(1), 30-44 (Eng). In dogs given a single dose of 5 mg./kg. of dieldrin, dicldrin concn. in the blood reached a max. in 2-4 hrs. and declined alter 10 hrs. to a relatively const, level which persisted for the following 22 hrs. AH intoxications should therefore occur within 2-4 hrs. after feeding dicldrin. In dogs given 1.0 mg./kg. of dieldrin for 5 days, 0.2 mg./kg. for the next 57 days, ami then 2 mg./kg. daily until intoxication occurred, the 1st muscular spasm occurred at a baseline concn. of 55 as-/100 ml. of whole blood. In both acute and subacute in toxication, the baseline concn. prior to intoxication was 02 as / 100 ml. After administration of the daily dose and subsequent appearance of intoxication, the ldood counts, of dicidrin were, resp., 74 and S3 gg./lOO ml. blood in the acute and subacute gtottps. The difference was not significant. Correlation be tween dioldiin conens. in blond ami body fat was 0.S4. The re sults support tin- hypothesis of a threshold level for dieldrin in blood winch, when exceeded, results in intoxication indepen dently of the type or duration of exposure Raymond ZUmpfennig 59116m Alteration of the locomotor activity of mice poisoned with sublethal doses oflead acetate, Tcrcm.A.L.; Vujkov.V. V, (Med. Fac., Novi Sad, Yugoslavia;. Arh. ffig. Rada Tnk- j:I*.','. 106?. I4'1 4 . -fill 'Engl. Injection of I'b'GAc'; m.-J-Jil ,;u. i.p.j ,.:to leu.jle n..ve \2l-uo v-i rr. -m.u Uu-e-de- pendent el .m ,,ii: l-,co:notnr activity. Singh do.-es p o.i-.-.g, d depie-Mnu of locomotor activity while chronic poisoning i u rea-cd locomotor activity. Single or multiple i.p. injections of saline did not alter locomotor activity. Animals poisomd with lethal noses of Pb(OAc): developed stippled cells during the 2ml or 3rd week while significant changes in locomotor activity were evident 1 day after the last injection. Mice poisoned w-ith sublethal noses (0.4-1.0 mg.) showed no stippled cells but display d changes in locomotor activity. P. H. Redfent K, OLI 5793 ; 1(1 ' *..*npn. i*l ll" K .in b*t\.i*li ill'!. | N, t'uii'-:.tnK.1'.. "Ciii.iii *' ; niiudlinii of IA*i damage raiiM-d by i..|\iii.iiin .!. ;i model of .-.ntihrpiuolnxin tbe/npy. );,t> i.nii'.... In m (lit**). In.i. Nl.nl.in ., (HI**1.* in , !.ini.-/('('*f iw. nim.r.i.: i.'.ir.'ii. Sikiii.n 111, t(<i|i*ii*' Oi l III in (lie scod- >*f Ai/i/unn linn innin, hi* t*ivie Hu is nf phalloiihn in mire. Rilyinnrin wax if in revet so. * iln* toxic cticri uf phalluMiii in nine * fnii wnli tbo niiiijnl, mid ilii-n tre.'tiwl with sily* "r (niiipli.illni'liii efiect of hill in.iriii depend***! on the 'jl tk'd'u i intoxication JiikI treatment, and on flit ytt damage. UQJG Evidence /or the biotetivation of elaframine. Alist, ' iMiflngnn Slate I'niv., East Lansing, Midi.). ISw- wiifiif. 1909, )S{4), 929-32 fliiis). Max. salivary 7 jniiliili.ir'mnI cmcsl itcl i/cd cats occurred *<**1 lir. j.liiiinixlr.Kitin of sl.ifrantinr (0.3 tug./kg.); the dma- . '-.ration extremely lone, usually lasting for 0 lirs. ..It* dose. In at)(In to salivation, most of the exocrine ..a specifically stimulated by slafraimnc. Upon ad- n uf slafrannnc to cons, sheep, and floats with pan- i-.aulas tin re was also a substantial delay before an in* piiiereatic flow was observed. lit mice, a longer delay jfirr i.v. injection of 2 mg./kg. than with t.p. adminis- ,*tne same dose; this delay v.a, decreased by injection -to the portal vein. Delay of the efTect of the drug at ,. was significantly extended by briefly isolating (with -,i* liver of rats; the effect was completely eliminated i.tnianrnt isolation of the liver. Common inducers of .i metabolizing enzymes consistently reduced the delay * MCtion of salivation in mice, while inhibitors of the en- idstcntly lengthened the delay. Thus, slaframiiic , require activation by the liver before stimulating exo* .ib. The enzymes involved in this activation are i (iio.r responsible for the metnbolisni of most xeier BYJN q Metabolism of phospholipids in the brain and liver i cuing intoxication Kith organophospherus compounds. i, V. Ya.; 'iofilu, A. 1'. (Pavlov Just. I'hysiol., Lenin- *jK). Byull. liksp. Biol. Med. 1909, G7t5), 50-2 fUtiss). '.u-.plionts compds, LG-G3 (A mg./kg.) and GA-K1 (0.4 administered i.ra. to rats did not affect tlic level of puls In the brain and ltvei or the rate of restoration of -nds in the brain. The metabolism of phosphotipids .(I was increased 24.fi'/, by organophoxphorus cotnpd. i-d 32.4 ri by GA-S1. The increased intensity of plios- xivtaboiisin may be connected in some way to increased if the hepatic cells during intoxication of tlie rlmlm- - ir.hilmor*.. IIJ J R ` I Toxicity studies in mice treated with l-A-n-arabino- 4'vtosine (ara-C;. Leach, William II.; Laster, W. )*; Mayo, Joseph G.; Griswold, Daniel I'., Jr.; Dank M., Jr. (Med. Center, Univ. of Alabama, .am, Ala.). Cancer Res. 1969, 29(3), 529-35 (Eng). * * therapeutic dosage schedules of l-d-o-arabinofuraiio- f tara-C) administered i.p. in mire (15 mg./kg., every 1 -'4 hrs.) result in karyorrhectic damage to the crypt * (ills of the intestinal mucosa. This damage is most ' I hrs. (earliest observations made) after the end of the "tw, after which there is a rapid recovery to completion ' The damage is thus transitory and resrniblcs that of "'(ia. This cycle of transitory intestinal damage fol- * Kcuitry occurs after each therapeutic dosage schedule *' lQI|g as the schedule is not repeated more often than I day. Progressive damage to the intestinal mucosa * ird by changes in the hematopoietic tissues occurs 'optimum therapeutic dose (15 mg./kg., every 3 hrs.) '"( uninterrupted to the LDu* dose (300 mg./kg. in `id beyond. Irreversible changes are seen in the in- ' uioi .'t, and a progri xsive depopulation of the Ixme 4mi ultimate ap! isia ensui ns the 1,1 do a* u le.ielu d . '""i. urn Lttect of butylatcd hyilroxytoluene (BUT) on rat ,. :'-me oxidase activitv. Pascal, Gerard; Terroine, "lr< Keeli. Nutr., C.X.R.S., liellevue, Fr.). C. R. ] ('IMI, Str. D 1969, 2d-v11), 1529-31 (Fr). The ora! II "it of MIT (I).u.y ; in the food, a Conon. AO-fold *n that aiithon7i-d for hmn.ut food) for S weeks e.uised ` ' * (fecrease in hepatic cytochrome oxidase netivity e. *r\es. Tin. addn. of 3H1T to rat liver lionioce- 1'' 1 of ]u e*.* e, l..\r ca'tsed a 12'. dun-asi m * (a -i .lei ii iii. 1 iu*. iAI .'.' ,:! .. duel on m vim niet.it*..l.a'i. Id Ji- wctivity of guanine deaminase in rat kidney, liver, 1 during experimental uianyl nitrate intoxication. , `""`v; Ifastidc, Pierre (Par. Mixie Med. Pliarm., Miraiid, Fr.). C. R. Aar. titel. 1968, lGJt.VOt, 1 I Guanine deaminase activity fll was studied in 'dney, and biood of rats during cxpll. intoxication niiii i*i mil oiti *i* ii ml i p, .l a *l*i ..... . i *, i*. I* **!y w (. |. A . i ai Iv n .,l I fo e laii i a pi*, i* ivi 11* . .*i i**o *.i ] w,. ti*ii**l in nil *'i...ii., Inn tliei wa n definite lowerin'; m 1 in tin l.nlin e f*i the lo I 1*2 hie. iifb-r lb*- stall iif inioxieatioii. Dinolhy J. ItiM'li loan llavnl.oo IIAl.Mai Pirn iii.n of ti*triii'thyl:*i-inniiiiiiin in the rat. On till!, J,, t'lnvef. gl , ).; )*lllt. I., U'llllll Iter'll. `I i 11 ,, t'.NMi.S., Tollfiilise, hi,). P. A*. Aw. /to*/. ]%lf, ItiJl.A (1|, li'.'i1* ll'rl; ef. 1'itet (I1H1T), hi.t.e Ml, n vety resistant eoiiiiiil. in vino, is ilre.indcd very enstly in the rat. Although 1 has a vtixy lug.li b.p., it is eliminated in large units, dnrini; rexpn.i- tion. `/ lie im inlxibii s of I found in n! urine arc GeOi nr Iln* germanates The melalHilisiu uf 1 is different from that uf tetra ethyllead (II) or tetraetliyltin (III). Nu evidence wiis found for thr formation of trieihvlgermnnium. which explains the weak toxicity of I compared to II and III. Dorothy J* Buchanaii-Davidson U3459v a-llydroxybutyrate dehydrogenase activity of rat kidney homogenate fractions alter experimental trranyl nitrate intoxication. BasinU', Jatiine; Bastille, 1`irrre (Kac. Mixtc Med. Pliarm., Clermom-Fcrrand. l*'r.). C. R. Sec. Biol. 1968, K12f8 9), 1492 3 ihr). Most of the o-hydroxybutyrate de hydrogenase activity of the rat kidney is found in the super natant after erntrifugation at 24,000 f for 2 hr*. This activity decreased with time during cxpll. umnyl nitrate poisoning, whereas thr contents of protein, DMA, and RXA were relatively low and underwent but little variation. C. W. Ackenon 113460p Effect of ethyl bromide on (he liver. Karimuilina, X. K.; Gizatullina, A. A. (Ufim. Naueh.-Issled. Inst. Gig. Profzabol., Ufa, USSR). Farmetol. Totsikol. (Mosceu) 1969, 32(2), 105-7 (Russ). EtBr fumes (2.4 mg./L) inhaled by rats and rabbits for 4 hrs. daily for 0 months disrupted the func tional ability of the liver, decreased (he hepatic glycogen and fat levels, and prolonged hexcnal sleep. Granular dystrophy in the hepatic cells and a decreased RKA level in the cytoplasm were detected. HJ JR 11346)4 Hemopoiesis in chronic heliotrine poisoning of "Wistar rats. Levin, G, R.; Novachenkn, 'i. I. (Uzb. N.mrh.- Isslcd. Inst. Gemalol. pereliv. Kravi, US.SU). Rnriiiatol. Toisiknl. (Moscim) 1969, 32(2), 170 1 (Russ), lleliutrine administered s.c. at 3-10 mg./lOo g. once a week for 1-S mouths to Wistar rats caused hepatic lesions, hypochromic anemia, severe rctieulocytosis, normoblastosis, and leukopenia. . Erythro blastic sprout hyperplasia, an increased no. of mitoses, and an increased no. of reticular and csp. plasmatic cells were observed. The observed changes in the blood and bone marrow suggest development of an autoimmune form of hemolytic anemia in response to chronic hehotrinr poi ionim:. BJJR 113462r Benzene metabolism in the liver of experimental animals and man. Tiunov, L. A.; Sokolova, T. I.; Hanriman, A. L. (US5R). Farmakot. Tokstkol. (Moscow) 1969, 32(2), 1HA-8 (RussJ. The rate of Cllt metabolism during 24 hrs. of incubation was similar in liver homogenates from humans and rats, more rapid in homogenates from guinea pigs, and slower in rabbit liver homogenates. Species-specific differences seemed to be involved in C)I, conversion, since the activities of aryl-4- hydroxylase and glucuronyltransferasc increased while the sulfonating system activity did not change in Cilli-trcated rats. In C.Hi-treated rabbits the sulfate adcnyltransferasc and aryl sulfotransfcrase activities decreased during disruption of the sulfonating system. The high rate of CiIIt conversion in guinea pigs may be connected with the relatively high liver catalase activity. BJJR 113463s Effect of the codium salt of adenosine triphosphate on experimental cyanide poisoning of rats (mechanism of the antidotal action). Moskcti, K. V.; Ganzhara, P. S. (Odcss. Med. Inst., Odessa, USSR). Farmakol. Toksikol. (Moscow) 1969, 32(2), 214-15 (Ru<s). Nu ATP (0.5 ml. of a 11,, soln.) given s.c. or i.m. to rats 1 hr. prior to administration of the min. lethal dose of NaCX prolonged survival. When given s.c. im mediately after lethal cyanide poisoning it substantially extended I he hie span of AH' ;, and prevented death in the other AO'T of the rat'. The uni Mode olTct of ATP may remit from it' ability to restore respitali**o by bypassing i-ytiuide sen-.ilive enzymes. BK JR U3464t Changes in the cardiac activity of rats chronically exposed to vinyl chloride vapors. Yazm, A. N'.; Plokhova, E. I. iGor'k. Naueli.-lSsled. Inst. Gig. Tr. Prof. Zabol., Gonki, USSR). Funonkot. Toksikol. I Moscow) 1969, 32(2). 220-2 (Ross). Chrome (A months) exposure of r.tlx to vinyl eldoride vapors at 0.113-0.(11 lug./!, disrupted cardiac work rhythm, in duced bradyrtrdi.i and arrhythmia, and -eiluecd the relative c.-r-o-.n *,f I_ 11 .o.nl T-ll (omul inurvaK. The relative rlura- x ii in i.i i..c yi ; i'i.';i;i.x d.d i *. . t .'a.:'' significantly. Within JA d.iys a'.'u ; leruMiiatiou of pmsouiue, the rat cardi.*c aetivily rhyiimi returned to normal, hut the duration of the I-II and 'J'-Il sound intervals remained below the initial level for another 1A days. The maximal permissible concn, of vinyl chloride apparently is significantly less than the 0.03 mg./l. level pre viously estd. BJJB . ** / A /g //jy&yt' OLI 5794 BbbU Co-....... ii Voi. 20, IOC'j fc ft . 1 ** it,. dally lot (ill iI.il . Ill' ll-I . il Imtli ,f and i rlnlinlili levi I . mil il> cleaved (In- nlItnmill In ilm! 111 j.iiiii, .1 rlitUilm level-, m u- imi affected. Ill: .IK 8581 Ih Effect of rclcnophene on liver and kidneys during carbon tetrachloride inlnxirntion. Xnlni.iii v-.lii. V. !*: Ttf.ari- nnvii, V. X.; MlUki-du-v-l.I,, V. K. (Mn-.l;. Mill. lust, tm. Srohcmiv.i, Mi now, USSR). pnriimLid. 1 nlnlid I'li'l' Srlruit, Motet. .Simp. 1967, Si 11 f Km-), "J ivn pinup- each rmn- prisitiR 1U inalc rabbits (2-3 kir-) unc used. All animals re ceived twice a week s.c. clows of 0J ml./kg. of a 40% oil soln. of CCU- To one of these groups 0.5 inl./kg. of ]% sclciiophcne coin, was s.c. injected 2 lira, later. During the 1st 10-12 days of CCU intoxication approx. 60% of the rabbits died in both croups. Selcnophcnr (6000 jtg./kg. approx. KM Mg. % or 1/32 of an LDh) protcetrd kidney tissue against CCU intoxication, but dystrophic and necrotic chances of liver were more extensive and more mjjsortant in animals to whom a combination of CCU with selcnophene was given. Thus, the rxptl. dose of sclcnoplicnc was too great and showed no protective but a destructive effect on the liver, althouch smaller doses of -3 ac. % of Sc arc necessary to maintain normal liver function. Addn. of 30 - % of Si- to the normal diet of rabbits picvcmcd dietary liver necrosis in cases of hyperthyroidism. R. Pavlak 85812j Toxicology of some polymers`(Povinolt). Dvoskin, Ya. G.; Kakhmanina, N. A.; Dcm'yauko, F. V.; Mcn'sliikova, T. A.; Erofeeva, L. F.; Lashkina, A. Y. (Xaucli.-Isslcd. Inst. Gig. Vod. Transp., Moscow, USSR). Gig. Sanit. 1969, 34(1), 7-11 (Russ). Tlircc samples o( poiy(vmyr chloride) polymers (povinols) conig. di-Ilu piiihalatc (I), trieiesyl phosphate, and chlorinated hydrocarbons as plasticisers, released 1 nun the sur rounding air in autts. of 1.8-3.73 mg./m.* in a scaled container and 0.63 during a single air exchange. All 3 samples had un favorable physiol, effects on exptl. animals and are not recom mended for use os finishing materials in shipbuilding. Exposure of sats to I (0.3-8 mg./in.1) for 1-5 days disrupted conditioned reflex activity and nonspecific immunity, and, to a lesser extent, x the blood protein cumpn. and phagocytic index, and the liver wt. J-induced changes were doscidepcndcnt. BJ JR 85813k Mechanism of boron effect on warm-blooded animals. Popov, T.; Angelicva. R. (Xauch.-Issled. Inst. Gig.. Sofia, Bulg.), Gig. Sanil. 1969, 34(1). 7S-S1 (Russ). Of 60 mg. B given to rats, tiic distribution was approx, as follows: 50 mg. in the bones, 0.G2 mg. in tiic liver, (MX) mg. in the kidneys, and 0.1 nig. in the brain. The max . was reached in 12 hrs. in the liver and kidneys, after 24 hrs. in the bones and brain. B w-as prin cipally excreted in the urine. Complete excretion of the ac cumulated B required a long tunc, but the majority was gone in 2 days after reaching the max. in each tissue. John Ilowc Scott 858Mm Effect of ascorbic acid on various signs of vanadium toxicity. Matantscva, E. I, (Inst. Gig. Tr. 1`rofzabol., Sverd lovsk, USSR). Gif. 7>. Pro/. Zabol. 1968, 12(12), 22-5 (Russ). 1.v. administration to dogs (8-10 kg.) of 3, 4, or 5 mg./kg. of ammonium vanadate, or 3-11 mg./kg, of X'a metavanadate in creased blood inorg. I\ glucose, and lactic acid, decreased blood glutathione, and caused salivation, dyspnea, increased respira tory and heart rates, urination, and defecation. Na ascorbate, 10-50 mg./kg. given i.v. simultaneously with, or 10 min. after the administration of V compds-, alleviated or prevented the toxic and biochcm. effects. One dog given 5 mg./kg. of both \ ammonium vanadate ami Xa ascorbate died of lung edema. The Severe toxicity of V compds. was attributed to increased vascular permeability and depressed glycolysis and oxidn. S. K. Vanov 85815n Comparative toxicity of some aialkylphenols and their quaternary ammonium salts. Gadzhibalacv, A. A.; Goryaev, M. I,; Dakhno, 0. V.; Kanaulova, L. F,; Potapov, S. V.; Slcpushev, V. S.; Churakov, V. I.; Dozorova, A. D.; Zharkova, I. 1,; Fcdrushkova, I, N. (Khim.-Tckhnol. Inst., Chimkent, USSR). Gig. Tr. Vrnj. Zabol. 1968, 12(12), -14 -7 (Ktlss). I he phenols p. and n-hydin\yili|)hciiylduurlh\ 1- tnrtliniie (I and II), /- and n-hydinxydiphcuvhiu-thvhnrthanc (HI and IV), tile tpi.item,try .Y-|,M,r (/nme(h) lbcu/ylpheunw )- cthoxy]cthyl]p,\ ridumim chloride lV), and a mist, tVI) of V and its ortho isomer hud m frogs the following LD* values: 334.0, 5S4.7, 320.0, 126.4, 42.5, and 42.5 mg./kg, V and VI were more toxic, presumably because of better water soly. which permitted better absorption. In mice and frogs II or IV first caused increased motility and convulsions, then marked central nervous system depression. All other compds. caused depres sion. All compds. applied topically to the -.kin or in the eyes of rabbits earned lo.-,d \ - ,i. .<::<! s. In rabbits skin absorption was c-vidiace-ci by the oeeurreiu. of toxic sums and death tm 2-3 mouths/ ailer topical application of 2b, 12, and 5% solos. f>. K. Vanov B5816p Tolerance tc lethal doses of metals in mice pretreated with low' doses, Voshikawa, Hiroshi (Nat. fust. Ind. Health, Kawasaki, Japan). Ind. Health (Kauaiahi. Jap.) 1968, fill-2), 88-6 (Eng). Rats were prctrealed with metal tons at 10% of the challenge dose. Pretreatment decreased the mortality after 4i ill. lire by Cd, I lg, In, mid J'h, ll.nl no Hlrrl with Mn mid ( n and iiii'iisisi-d inortabiy in Fciiiul Xn. When the cliallenio* nm , was different (rom the pritrcaiinciil metal, Cd, llg, In, and l'p developed cross tolerance. I), Barbara Sankar M58l7q Bevcrr.ible necrosis in striated muscle fihci* of tlo rat after scveie im.,mention with various cholinesterase inhih itors Amiis. A. Tli.j Cohen, It. M.; Meeter, H.; Wnlthtn, 0.1.. (Med. Hud. J.ab., Xat. ltd. Res. Organ. T.N.O., Kijsu tjl Nelli.). Ind. Med. Srt. 1968, 37(11). 845-7 (Kng). Albino rats (200 g.) were injected i.v. with just tublcthai doses of paraoxon, diiaopropyl pliosphomfluoridaie, or tabun, and saeri ficed at various intervals alter injectton. The diaphragm, intercostal muscles, gastrocticmius-soieus muscle group, and :h, psoas muscle were dissected, fixed in 10% lunnalin, and examd. histol. I-oral necrosis of muscle fibers is caused by the ah normally long-lasting presence of acetylcholine around the end plates. Muscle fiber necrosis may also occur in man alter an ii cholinesterase poisoning. R. R. Rowlands 85818r Chemical Mace: ocular effects in rabbits and mon keys. MacLeod, Ian F. (Med. School, Univ, of Michigan, Ann Arbor, Mich.). J. Forensic Set. 1969, 14(1), 34-47 (Eng) Direct cornea] contact with liquid Mace produces lasting opacities and melanosis. Spray exposure resembling that anticipated fnt actual use of a Mace weapon cause* only transitory lesions of tin face and eyes with possible tunburnlike scquellae. A Mace weapon should not be aimed directly at the face if it is discharged at less tliau 6 ft. The propellant docs not seem to lie rcspon-ihle for the injuries; they teem to lie due to the lacrimator, clilnrn acetophenone. Irving Sunshine 85819* Cerebral amine* and acute hyperbaric oxygen toxicity. Blenkarn, G. Douglas; Schanbcrg, Saul M.; Saluman, Herbert A. (Med. Center, Duke Univ., Durham, N.C.). J Pharmacol. Exp. Ther. 1969, 160(3), 346-53 (Eng), Acute central nervou- system (CXS) toxicity impedes treatment with hyperbanc O (OHP) for ischemic illness which led to a study of relations between cerebral amines and OHP-induecd CXS toxicity in rats after in jection of selected drugs. Brain levels of noreninephrine ami serotonin were unchanged after 1 hr. of OHP at 4.95 atm. ab= Injection of pargylinc (40-60 mg./kg.), a monoamine oxidase (MAO) inhibitor, 30 min. prior to OHP (4.95 atm. abs.) exposure for 2.5 hrs. increased (54%) the latent period before the onset o! convulsions, decreased the frequency of convulsions from 92 m 33%. and increased 72-hr. survival (rom 20 to 59% (n " 60) Iproniazid (25-75 mg./kg.) proved equally effective; isoniazid (50-100 mg./kg.) was ineffective. Although inhibitors of norepinrphrinc synthesis (-methyi-/>-tyrosine. 100 mg./kg.) ami of 5-hydroxytryptatnmc synthesis (DL-p-cliloropliciiylalaninc. 300 nig./kg.) lowered reap, amine levels without changing 01II' tolerance, the protective actum of pargylinc remained unaltered. Amine precursors 5-hydroxytryptophatt (10-25 mg./kg.) and 3,4- dthydroxyphenylalaninc (25-50 mg./kg.) also failed to alter O tolerance. The data indicate that premedication with certain MAO inhibitors can protect tats from OHP-induced CNS toxicity. These studies suggest that both the CXS toxicity in duced by hyperbaric O and tiic protection from toxicity afforded by certain MAO inhibitors are not mediated through alteration- in the brain metabolism of norepinephrine and 5-hydroxy- tryptamine. RCHP 85820k Effect of Coprinus atramentarius on the metabolism of ethanol in mice. Cohlwcll, Blake 11.; Gcncst, Klaus; Hughe-. David William (Kcs. Lab., Food Drug Dir., Ottawa, Can.). / Pharm. Pharmacol. 1969, 21(3), 176-9 (Eng). The Eton-V'! material extd, from C. oiramenlanus was more toxic to mice, a- measured by the LDm and potentiation of the EtOH-indmvd sleeping time, than the whole mushroom or the residue remaining after EtOII extn. Also, the EtOH-sol. fraction when fed to mice 4 hrs. before administration of EtOH markedly increased tin blood UAc and EtOH levels. RCII'J 85821m Salivary gland regeneration after m,-ethionine poisoning, rimansky, Mario; Knhinim, A.; Unear, lleni\ (lladas-ah Mul. Sell., llelurw Univ., Jerusalem, Israel), /.a' lnvr\l. J0G9, l/i>i/l), 231) 3 I Fin:)- After elhioume feeding, thi i11 is mere.i-eil strueLur.il damage during the first 24 hrs. to t.11 salivary glands of male white rats. Recovery begins in 48 Ut - After 72 hrs., mitotic figures are apparent, and after cessation cthioninc feeding for 2 weeks, morphological and histochcm indicators of the salivary glands are normal. Anna I.cc Waldo ^ 85822n Changes induced by cadmium, zinc, and lead in sen-and peripheral vascular resistances in the anesthetized rak' e k-1|.[ 11!*G. remain; C'o-i;mtitii. 5.. Oir.a. A. M. 1 Milano, Milan, Italy). Med. I.ttl. 196S, 59.8 !)'. 522-;>3 1 K. Cd at lmJ-50U ag. into the jugular vein of ancstnvured ra" produced a urop in the vascular resistance of the renal an. which decreased approx, with dose in magnitude and dur.it At the highest dose it was almost absent. The effect mi > arterial system below the aortic bifurcation (measured at carotid) varied. There was an increase in vascular rcsistann low dosages and a slight redn. at higher dosages. Ztt and 1 u ' ) n / -7 V / J OLI 5795 f i s* A 'f ,4 -'f, A H i I '.fsir J 1 1 20M.J Muffin .) Ah\h;n I Vitl i.M. coiiijhuh nlr: tif'Ctl In nuimifrtit* i.f tlr C,in .., S.1 H.itx irt.in, !>. I*. Kmvx.mi, It, L. W. 1.. .mil h*lni AtitiiMi (I'litv. if 1 rims, Att.ldi) An.fr. J. //**/*, f'famu. 2-1 tit). I'.I | .VH (litiiT H I'JI;:). *| lie ! *hmi|in, ii-.rlul in rlilii! the MtLtlc toxicity of Rome inKrvtlivnK iti tin muiiuf. of po)y(viuyl cM*riiU*) pLiMifS, mmiI tti thr *f coin,liner * AIkI ckNIKl. (or r<Tlaill I|u|u)`hmK, utr ilmi .Mil. of detection inrliiik tissue eitltmc tests. iiiini.il expis., ami elltvts On nnli!x*ly rend ions ami mi wa^linl Id* mil rrlls. CYrt-un heal ftabilizcr* rJnmetl a marked iiicmupntabihty with the hint, systems tiled. Reactions with 5 phstisizcrs were more subtle. The results suggest the need for further research into the relations between various levels of toxicity and potential harm in humans. II. M. Hmlaiy* 2056 Ir Some chemical aspects concerning the occurrence of aflatozin in foods and feeds. W. D. Raymond Clro|i. I*rod. Inst.* Loudon). Ann. 1st. Super, tentta JfPt* 3-1), (19G7)(ltal). This paper reviews various aspects of the problem afUtoxin in foods and feeds. The agricultural, inycological chcm., anal., bioehem., toxic, com., and public health aspects of the problem arc discussed. The presence u( inyc'otoxius in foods and foods also is summarised. 47 references. Katherine 11. Fisher 20562s The effect of diet on carbon tetrachloride metabolism. A. A. Seawright and A. . M. McLean (Med. Res. Council Labs., Carshulton, Engl.). Biochem. J, 105(3), 105.VG0 (19G7)(Eng). Blood and liver concns. of CCU were measured at intervals after an oral dose, in rats given stock and protein* free diets. The values did not correlate with the resistance to poisoning found in the rats given protein-free diets. Metabolism of CCb to COi in vivo and in liver microsomal prepns. was de pressed in animats given protein-free diets. Rats given a single dose of DDT are highly sensitive to CCh pniyiniug. The livers of such animals had an increased microsomal protein content and greatly increased microsomal activity in the dcmcthylation of Pyramidon and in the conversion of uCCh into "COs. The incorporation of leucine*14 C into protein by liver slices is de pressed by CCh. This vfTcct is decreased by the addn. of SKF &?5A and in slices from rats given protem-frev diets. It is suggested that the toxicity of CCh is closely linked to its metabo lism. RCFG 20563t An attempt to influence the collagen defect in ex perimental lathyrism. K. Truavsky, Z. Trnaviku, B. Skruvina, and L. Cehecauer (Res. Inst. Rheumatic Diseases, 1'iestaiiy, Czech.). Biochun. Physiol, Tissu ConjonchJ, Conf. Comuiun, Syrup. Ini., Lyon 1665, t>C3-70(]*ub. 190G)(ing). To study the influence of hydrocortisone (I) and Na salicylate <T1) on the soly. of collagen proteins and on changes in the epiphyseal growth plates in lathyric rats, cxptl. lathyrism was induced m 30 male rats by feeding a 60^ concu. of sweeipca seeds (Lathyrui odora- tus) for 30 days. Twelve of these rats were simultaneously treated with I (10 mg./kg. body wt. daily), i.m.; another group of 12 were treated with II (2o(> mg./kg. daily), i.p. The 3 Cxptl. groups were compared with 3 noiiiaihyric control groups treated similarly. Afu-r 30 days, total hyilroxypiolmc (III), dialyznblc III, and acid-sol. Ill were deld. in dorsal skin r\ls. For histol. evaluation, the tibial growth plates from decalcified hind limbs were microscopically cxumd, 'iotal III was not significantly changed in any of the groups studied. 1 in intact (control) animals resulted in decreased levels of the neutral saltsol. Ill and dialyzable III. II hud no effect on the sol. fractions. Feeding with sweeipca increased the neutral and acid sol. Ill; the greatest part of the lathyric neutral sol. fraction being dialyzable. In lathyric rats, 1 treatment depressed the elevated amts, of sol. Ill as well as dtalyzuble III. Even more effective in restoring normal conditions in lathyric rats was II treatment. Histol., the cells of the epiphyseal plate in lathyric animals allowed elevated mitotic activity but delayed maturation. The synthesis of ground substance in the intercellular spaces was also disturbed with demasked collagen fibers, granular deeompn., and some cystic areas. I depressed lathyric toxicity, while II restored the libial growth plate to nc.nly normal. 1<) references. L. K. Allen 20564u Toxicity of 1,2-diehlorocthane-extractcd fish protein concentrate. 1, C. Mimro and A. 11. Morrismi iFoml Drug Res. Labs., Dept. Natl. Health Welfare, Ottawa). Cu. J. Bioihern. 45(11), 17T`J-Sl(lPG7)(Eng); cf. Cl 67: ol'SUM. WUtar rats were fed a protein-free diet with 50' i protein from lyophdizcd or extd. cod fish (lyophih/ed cod extd. for 1M hr**, with bo-PrOH Or 1 .--dichlormt h.ivc \ I hen h" ife<l f**r :* It* *i 'to v.o-uo > which contained 4W mg. sl.jm'i-cnoliio *..M`<iide ii, Lod fillets extd. with I wort toxic to the growing rat. * he toxioity was not due to II but was cuu-d. in a MeOH e\i. of the I-trcatcd fish. However the MeOH-cxtd. fi'.li did nut support growth even when supplemented with cystine and histidine. Dorothy J. Buchanan-Davidson 20565v Significance of carbon monoxide from cigaret smok ing inside a car. Milan Srch (Karlova Luiv., Hrader-Kralove, Czech.). Deut, 2. Cesarnte Genchtl. Med. 60(3), 8')-f)(311(57) (Ger). A forensic opinion from the author was netded in the r.i j1 t*f ii .'til v* -ii ..lil w..iii.iit tvlm It.ttl ili*il in i. ri,, IVM.ir..' Ill .1 II -I IIII *1 |rt I `.HI'.. 2 .f III. Ill Mlliil.r|, IIII,I . un.il,fi Him *^il in :i rlir-.'il nn willi n rllliulttrr nf */ h illi'l slimkril ,ri cl;:,lift'. Hllli llllllll.ltliill llm mi; (M) mill,, I),, licnmi-.liilim cuttrti. ill the lilood of the unnkm rose [r,,lu Itf'i. that in 111.* hliMhl nf the niiii.iniki'rs from *2 In .V,'.. r Mich i`iii'mii'.t.inivs n f.ilnl nilinif.itinn \\IIccmci] III,t |MI C'.niM'iinciici". for tnilhc Mifcty are tlmivnl, 1). J|, st<, 20SOiiw lIiKtn>iutor.iilio|,r.'i|ihic ttuilicr. on inetcnchyin.il duct edit of thionccumide-iniiuccd cirrhotit of the liver in i BaJlhatar Wohlgemuth (Karl-Marx-Untv., Lcipiic, (, Exp. Pathol. 1(1), 04-71fl907)(Gcr). Wliite mice (IO-lwcrc fni 0.25-0.45 m)t. Ihioacetatnidc (I) in the drinking u Cmitriil. without I were trrsitetl further by the same prin'cI After 711 ilays the animals were injectcil i.p. with 2/.ti. nf n, dine (IIy-'II/g. body wt. After thir, the animals were i amt the liven were lixcd m HCHO; acctions (5 m) were v,., .with inactive U to remove unincorporated IIJH, and amn- Itramt were exposed (or 4, 0, 8 and >B days at 15'. Af: . days tlic devciopnietit of cirrhosis had proceeded widely treated auimals. Ttie pnienchyma was penetrated by ren ami collaftenous fibrillar structures at well as with mcsciiclr and duct cells, which increased in relative no. The incui, tion rate of II-*// into bcpntocytes increased from 0.03 (mm to in cxptl. animals; in KupfTcr's cells the resp. bl; indexes were 1.G7 and 2Al'~,. Labeling of hepatic capMil. endothelial cells or of the bile duct epithelium showed m> fcrctice between controls and I-treated animals. The duct exhibited a labeling rate similar to that of Kupffcr's eell\ treated animals. As early as I hr. after II application, black mitotic figures could be seen in KupfTcr's cells, both in com and in I-treated animals. A possible shortening of tie pltasc due to unexplained reasons was considered. 34 rtfere, E. Talafai 20567X Histamine level and histamine fixation in the 1 tissues and skin in rats under the effect of industrial pob R. S. Eixcngart (Sanepidst., Moscow). Formakol. Tok 30(5), fi08-!)(10G7)(Riiss). Homogenates from rat brain from rut skin were tested chromalographically for lnst.i concu. and histamine fixation after rats had been exposed i to threshold concns.. or to toxic doses of mcthylcyelohc ethylene stilfide, diclhylatninocthyl mercaptan, or 2-iuctl: vinylpyrnliuc. At threshold levels there was less hista; fixation in skin and more in brain tissue. After toxic h the changes were irregular both in concn. and in hista: fixation. Julian F. Sun: 20568y The toxic peptides of Amanita phalloides. Tin Wielaml (Cscthc-Univ., Frankfurt/M., Ger.). Fortschr. C Org. A'aturst. 25, 214-50n9G7)(ling). A review is given: mushroom poisoning is almost exclusively attributable to t. bers of the gcuus alwinmla. Their toxins are completely sorbed from the gastrointestinal tract, while tlicir acti, primarily on the liver; no specific therapeutic agent is kuna present. Thus, the understanding of the chcm. structure the mechanism of the action of the toxins is of great import from the therapeutic sl.oiilpuim. Isolation of the loxu gredieuts, the client, structure of the toxic peptides, the j foidiii nud the umutiitiii group, and synthetic expls. with a acids and cyclopeptitlcs arc covered. KG references. CS, 205691 Comparative toxicity of mercaptobenzimidaxole its line salt. X. V. Mezentseva. Gig. Otsenka Khim. Fai Vncsh. Sredy 1966. 119-20(Russ). Mercaptobenzimidazoi and its Zn salt fll) were studied tn acute (mice), subacute (; and chronic (rabbits) expts. LD internally for mice was for I and 737 mg./kg. for II. The animals were exposed and II dust for 2 hrs. daily for 15 days in concns. of 401) : m.* A lug in wt., increase in the content of amino X in urine, and disturbances in the nervous system were obstr Morpliologic.il alterations were found only in the lung tissue > bronchitis with slight atrophy of the bronchial mucosal chrome expts. on rabbits I caused disorder in the protein.' ing function of the liver, II increased the lipid cunlcui e blood. 1 increased the aldolase content, and II dccreusi cholinesterase activity of the blood. I decreased the crythn count in the blond to 20,000, A proliferative reaction was : in the lungs; edema and fatty dystrophy were observed i liver, and punctate hemorrhages were observed in the cartlium. II caused slight edema in parenchymatous o' I had no irritating ellcct on the skin or mucosa of the whereas II caused moderate irritation. From RH Zh.. F''-rl Amnngerue. ,'itcdy.a. Tohukol. 1967, Abstr. No. 7.54.Sol MV: 20570t Methods for the qualitative and quantitativ: termination of afb.tozins. E. II. Marth (Univ. of Ww Madison). J. Milk Food Technol. 30(10), 317-20(1007d : Qual. and quant, measurements of aflatoxins by means oi layer chrmnatog. can be improved by substituting a ils metric "reading" of the thin-layer plates for visual f lixamn. of small samples (down to 0.3 mg.) can be accomp by a thin-layer chruiuatog. procedure which employs a .< OLI 5796 ( |l'l|l. -Il Al' ,(l .11 I . V.it 1/1, I'li.r. 4I I r tv irk, N.J.). f'riw. J. I'l.ynol. /'/ <mrnt it!. I OOS, I'm I ], is r I Hi Is-.led, Inst. Onkn!., I.ruincrutl, USRIt). pormoLoI. Top (Klip) A si lies iif rspls, ltd slow it that tit* in, ; h 011 tits liy 1'Mih. 3IC;r, biil 5 (Rii'.s). Pol)etliyii'iii1 |h-ly.1 r 11 tin- (7.V) 1 Wllif It lilt* Ilir'Inlloll'.UI Ilf I* 11 tl I *11 rill .ill' Mlon.'.l} III till, 111`I il lit' Lr..l iidiiiini .ten'*! i..r. in tal'. mill inii'i- iu>*ri-.ra.| th.- I,.', till' plllll.ll (III''.1 Ill I11. Ill till- tl Jill I'lll III III, .lll.tllll- III! lltlllll . mono mini, owdii j- niiil lii'.i.iiiiiii.i'.r nelivilie .. fierii-.ism;' f*m tin- H1* isI liri|in`iilly ii'.i'il gas mill., tl.1/, *i. */,' I'll,-, I>1. 111111 and hislaiiuiu- levels tu thv blood and organs ol tlir Hit>11 rtniMiinptMiu wax abnormally Lifi.i . :inil pro|Mirlion.il |nil.siiui'd animals. 'idle jtatho!. disturbances observed in n to the CiHini. of ElOll ill tin1 pi-rfusutt, lln.vi nr. when tlic and rats with acute polyethylene polyaminc poisoning nu\ syttcm was aerated with IS',1; O, + CO: + 77',, N;, the due to the increased oxidative deamination of endogenous am consumption of EtOIl Was similar to t'.ia* found ill tlir mtacl with tin- couscqiiciil formation of aldehydes. XIlj, and 11/) rat. f lic jiilfusiK eiineii. of McjCt), HOAc, fiytnvie acid, a:nl BJJI lactic aeitl was measured in all cxptx. When I'.tOlI was con 50598w Effect of niacin on phagocytosis in ehronie trim: sumed at these two (lifTercnt rates, increases m the lactic:- toluene poisoning, l'idcmskii, E. L.; Chukichcv, E. pyruvic ratio and acetate levels of the perfusate sure noted Mul'imnho, A. M. (Penn. Univ., Penn, USSR). Paroin: in both tyjies or expts. However, the utilization of Kiurnse Toktikol. 1968 , 31(3), 3C5-G (Russ). Trinitrotoluene (T.'. by isolated perfused liver was inhibited, and acetone levels in administered orally at 30 mg./kg. daily (or C days to rats |. creased markedly, when EtOH was consumed at almorm illy rapid grcssivily decreased phagocytosis. Xiacin administered sin rates, although no effect was noted in the perfusate levels of these laueously at 1 ing./kg. s.c. prevented this decrease and even metabolites when ElOli was consuinnl at normal rales 27 creased the phagocytic activity of the leukocytes to 1.5-tunrs; referenets. 1<CVI> level in control ruts. BJj): 5059Ip Action of beryllium ions on primary cultures of swine t 50599* Pathogenic effect of chronic exposure to vinyl chlon cells. Vcgni Talluri, Maria; Guiggam, Yivrana lUmv. Siena, on rabbits. Vatin, A. N.; Piokhova, E. I. (Inst. Gig. Tr. Pi. Siena, Italy). Caryolozia 1967, 20(4), 355-G7 (Eng). The zabol., Gorki, USSR). Farmakol. Toksikol. 1968, 31(3), 3' efleet of Be44 poisoning on mitosis and morphology of swine 72 (Russ). In rabbits exposed to vinyl chloride (9-10 mg kidney cell and lymphocyte cultures was studied. Treatment with Be4"4 had a harmful effect 011 all the miiotir phases and abnormality of chromosomes was frequent. At high conciis. air) for 4 tin. daily (or 5J5 months altered d-waves (frequen, >80 llz!) appeared 011 the electroencephalogram from the tirmr hyiHitlialailiic nuclei, and the potentiaK of the ntitvi the action of Be44 was less pronounced on kidney cells than on and posterior nuclei increased by 1S-30 and 70-85' ;, rcs|i., m lymphocytes. Be44 exerts its toxic action liy compelilion control vnlucs. Concomitam changes ill the cardiovascular m with Mg4+ cither in the activation of DNA polymerase or in lent (bradycardia, arrhythmia, decreased voltage of the i- the binding of DXA to histones. L. Mirouc dividual electrocardiogram peaks or whole complexes, dccrea- 50592q Protective effect of ethyl alcohol towards ally! alco duration of systole, increased arterial pressure, and retard, hol-induced hepatic lesions. Schwarztnann, V.; Infante, R.; blood How) also occurred. The functional changes 111 the a Raisottnicr, A.; Carol), J. (CHI) Saint-Anloine, Paris, Fr.). tenor mid posterior hypothalamic nuclei may have a role in t C. Jt. Soc. Biol. 1967, 101(12), 2426-!) (Fr). A 90-inm. per pathogenesis of toxic angioncurosis due to vinyl chloride. fusion oi isolated rat liver with blood contg. allyl ale. (0.018 ml./ , 180 ml.) caused a release of lactic dehydrogenase, malic dehy BJJR S0600r Brown FK.. HI. Administration of high doses 1 drogenase, and glutamic-pyruvic transaminase into the perfusate rats and mice. Grasso, P.; Gaunt, I. F.; Hall, D. Golbcr and a simultaneous depletion of these enzymes from the liver; L.; Batstonc, Elizabeth (Brit. lnd. Biol. Res. Assoc., Carsha ale. dehydrogenase and glutamic dehydrogenase activities ton, Engl.). Pood Cosmet. Toxicol. 1968, 6(1), 1-11 (En. were not detected in the perfusate and were not decreased in the Acute oral toxicity studies with Brown FK gave LDa values y- liver. Biliary secretion was irreversibly arrested after 1S-20 g./kg. and 8 g./kg. in mice and rats, resp. The values for i.; min. of perfusion, and hepatic lesions occurred. A 20-min. per injection were 1.5-2 g./kg, in mice and 0.75-1.15 g./kg. in rat- fusion with blood contg. FtOH prior to the treatment with allyl ale. prevented the enzyme release, the hepatic lesi ns and the effect on biliary secretion, and aid not cause the release of ale. dehydrogenase or glutamic dehydrogenase activities. BI'JF When repeated daily oral doses ranging from 0.1 to 2 g./kg. wc: given to rats, a precipitous wt. loss and a vacuolar myopaiN of the heart ond skeletal muscles accompanied by hpofusc formation occurred with doses of 0.5 g./kg, and over. At tl 50593r Effect of ethanol on hepatic metabolism and enzyme highest dose employed (2 g./kg.), there was also hepatic centr activities. Kelson, Patricia Ann (Indiana Univ., Blooming lobular necrosis and renal tubular degeneration Pretreainnn ton, Indiana). 1967, 104 pp. (Eng). Avail. Univ. Microfilms, with antibiotics reduced tbc incidence of muscle lesions. R' Ann Arbor, Mich,, Order No. CR-722S. From Din. .)b\!r. B prated i.p. iuiectiou did not have any effect on the heart or skclr; 1968, 28(11), 4088. SNDC 50594s Energy-linked calcium transport in liver mitochondria during carbon tetrachloride intoxication Carafob, Ernesto; Tiozzo, Roberta (Univ. Modena, Modena, July). E\p. Mol. Pathol. 1968, 9(1), 131-40 (Eng). In rats intoxicated by the gas tric intubation of 0.5 ml. CCU/200 g., Cn,+ coueu. in liver mito chondria increased --10-fold within 18-20 hrs. However, i.p. injected 4iCa was not taken up by hepatic mitochondria in in toxicated rats as rapidly as in normal animals. In vitro, hepatic mitochondria from CCb-mtoxicated rats did not show increased n Ca'* uptake, but Ca*4 release induced by oxidative phosphoryla muscle. Only 2 of the C cont|nwients of Brown FK, 2,4-diamim 5-(p-siilfnplieuyla/.o)ti)liieiu' (1) and l,3-diamino-4-(p-siili phcuyl:i/.u)beii7cnc (II), produced muscle damage after repentr Oral doses of 0.5 g./kg. Comparable doses of mists, contg. tl, oilier components as well as I or II were considerably less toxic After daily oral doses of 1 g./kg., muscle lesions were found : rats, rabbits, and guinea-pigs, but none were seen in mice 0; hamsters. The results suggest that the intestinal micoflora : responsible tor the breakdown of the components of Brown FK to toxic pruducls. Variations between species and between an mal of the same species may be due to qual. and quant, dn tion uncoupiers was greatly decreased. This suggested that in fmnecs in the intestinal microbial population. RCXI* Ceil intoxication, the balance between AI>P phosphorylation and Cn,+ uptake is shifted in favor of the latter, thus contribut ing to the accumulation 01 Ca1' in mitochondria. I_)J)JN 50595t Protective effects of alpha-tocopherol 011 the hepato- toxidty of carbon tetrachloride: an electron microscope study. Meldolcsi, Jacopo (Inst, Pharmacol., Univ. Milan, Milan, Italy). Exp. Mol. Patho!. 1968, 9(1), 141-7 (Eng). The oral administra tion of 2.5 ml./kg. CCbdild. 3 .2 with Jirj. paralhn to rats produced severe hepntic lesions within 24 hr... However, liver il.on.ter was markedly reduced in rats i.p. nijeelid with the lipid autiosnl.im, ei-tocopherol sueetnale (I2o 1111;. kg.), hefoie Celt aihitinixiru- tion. Tins suggested tlut hpnl perovidn. is the piimary rneelu- msm of CCl* hepatoloxicity. 27 referenci s. j)DJ\ 50601s Brown FK. IV. Cytopathic effects of Brown Fj on cardiac and skeletal muscle in the rat. Grasso, !'.; Muir, A. Gnlbcrg, L.; Batstonc, Elizabeth (Brit. Inti. Biol. Res. Assoc , Carshalton, Iingl.). Pood Cosmet. Toxicol. 1968, 6(1), 13-2 (Eng). Administration of 2 or 3 massive (1 g./kg.) oral don of Brow n FK to rats induced a myopathy in cardiac and skeh't., innsclrs charactm/rd by multiple vacuoles --1-2 a in diam Ulttastnu'tiirally, these consisted of areas of librillulysis, .r feet mi: initially the A-h.md. Ihstocltcm,, the myopathy w., acisimiMMn d by a model.itr im'ti i-,r in arid phospjMlase acto'il i and by a loss ol pliospliniylasr activity. Subsequently, complet lysis of the alTerted libers ensued. In the heart, lysis was fol luw'td by macrophage invasion and fibroblastic proliferation 505%u Distribution and toxicity of aliphatic hydrocarbons in and in skrI1t.1I muscle, by'regeneration. The occurrence r, body tissues. Slmgaev, 11. I), (Yntinl.iv. M ed, 111 st., Yuroslus 1, lipofusem in muscU' fibers and in macrophages was scanty an USSR). Idnnokol. Tokstlol. J908, .'licit, .`hid ,'t tlinsey (las erratic. When lirow-n J''K was given m the diet at a level of 2' . chromates. was used to study the distribution of ti volatile hy fibrillolvsis and an increase in the no. and electron cl. of ly-o drocarbons in the mouse and rat body tissues. The volatile sirims was ob-rrvrd ultrastructnrallv during w-eek 2-3 of i'1 hydrocarbon content r>t the l.crn ro:d ............... , ,., : u, 'j'lu-t e/iuiue-, weri aeconijiamed t))r a nurked clevat.,. was Mil, 11 j:. but toe iev. ! m Lite tatty p.-ne a.is m-iiil.e only ol jii.iocitem, demonsttable acid phosphatase, l'ro..re- n * higher than in the brain, Imr, k'diiey-, or .-ii.'eeu. J i.,a w is a ih posit mu ot lipofti'eiu was tlie principal pathological featur parallel between the toxicity and iftietui eeithial eutte-.t. of i-o- dm tit,: week 3-12. initial damage to the A- and 1-bands til but1 prcnc, divmyl, and isobutylene, but not of butane, J-meih;. Ipent- cardiac and skeletal muscle distinguishes the- Brown FK myop i-cnc, or 2-mcthylpcnt-2-ene. The divmyl coneu. was higher in nthy from that known to be produced by high doses of corn the medulla oblongata than in the cerebellum or cerebral cortex. costeroids, thyroxine, chloroauinc, or plnsmocrd, from ischem. BJJK damage and from muscle damage resulting from deprivation u 50597v Some biochemical changes in animals following acute K, Ca, or Mg. The lysosomal changes and accumulation o) polyethylene polyamincpoisoning. Solomtskaya.E. A. (Nauch.- lipofuscin are suggestive of primary lysosomal damage wind OLI 5797 i, ,M< jin . .*! . n>. |w- * <*1 * I V * in nulls **III il m.i.iimh, , #U0` Mammalian I'.illn,logical Ihoeheiiii'.li) , Nt'linit 12. `,f synthesis **f 1-*' ....................... iflt lit -x-.li-in lor 'siiilhexis prcpmcd limn lytirfrli Imdc mu i*.-omnl vc..iele. '.lllllirMIII iLllmullt ll.l *1(111. Ilf . Vr **f I">lv."ill-'I1.1. **f Nlhnnn* ll.l '-IIIIM.Ul 1', ' j1,, salmonella (Sect. 2) 1E7V01. Tn|*oc)icni. nuungcimnt IcauIcs in erythrocyte membrane (Sect. 2) 18S08h. ' ,i jiivr sillily ol reaction of In-paiin with kcxntiimmc Colxilt H- ami lysozyme (Sect. 2) 18724c. Ascorbic acid oxidase , j from different plant materials (Sect. 3) 100041. Effect -ii.mc prepu- on protrill fractions of immunized animal * .Seri. 4) 19263p. Changes in body cmiipti. during lotig- irvjtnictit with cortisone and anabolic steroids in astlnnatic ,,t, (Sect. 4) 101881. Simplified hatch method for isolation "glycoproteins from normal and pathological scrums and ViSeci. fi) 19409r. Biol, activities of polyelcctfolyiic.dly ,r mactoinols. (Sect. H) 1971Ih Immunnclcrtroplinrclic antigenic coiii)>oiiciits of Bacillus mega terlum (Sect. J. 1 I V7 V/i ; . ,.|. .Old i II II a II i It il loll ol col mil no`. Ii o* 11 ji* tl * iiOipofli III'. I,1-el. >1) 107 |(i|*. .' ill In I III' :i In) tliicli,.. of Jollioi- t>|........... Ill .nit llnelv III mull1 Ill'll. IVMfip I fill* II oer Ol pio 1i'ol)tic nrlivilv of spl(.|-n cell, ill young ,nid loiiniondogic.illy In 11 uie r.difnts fiScel. Ill 20213d. Cm (fcoslcrdid-tnuihug eI..1 ml II liim lii HO IK , phy ioloi y, and phytogeny tlv i l. 11) ZPIhil. I>|.|i'i"iion of rinbiyii.s|MTitie globulins in m'iuiu or I'lnln viii mill flltlleiin Itlilllall inf.nils (Seel. II) 201 ftOf. Ciiinp.native liuimiUdghiliuliu flelns In hllln.ill heillin (tied. 11) 20178w Sensitivity to miiiic fungal allergens during penicillin piepn (Seel. 11) 20587d. Hole nf histamine in production of iimiiediate reactions of wheal and angioneurotic type (Sect. 15) 20r.54p. lifTs-cl of some ganglion-blocking prcpils. on dcvclop- III. m and course of anaphylactic shock (Sect. 15) 20830c. lnllo* on of rhlr-ramphcuicnl in immune reactions in rats (Sect. 15) 2us0bz Methodology and trends in study and prevention of air pollution by chctti. allergens (Sect. 50) 15779p, Antigen with nucleoside determinant (Sect. 63) I6099d. Fractionation of steiiificaiit quantities of hiol. active prepns. by prolonged pre- li.ir.itivc- pajicr electrophoresis (Sect. 2) 18711w. Kcsponsc of lyioplncytes til penicillin; comparison with skin tests and circu lating antibodies in man (Sect. 15) 20700s. 14--TOXICOLOGY T. a. TORKCLSOM ,;:M6q Chemical analysis of aflatoxin. R. Monacclli and Study Drug Toxicity 8 93-10G(1907)(Eng). The report sum i tl. Manzone (lust. Su|icr. Sanita, Koine). .Iw, 1st. Super, marizes the behavioral effects of anticholinesterases, and evalu .m 3(l't. 3--1). 31C-20(UM17)(Ital). A review with 23 refer* Antonio A. Kixzoli ::S47r Toxicity of mercury vapor. G. A. Neville. Can. ates the usefulness of behavioral methods for toxicological in vestigations with Para-oxon, parathion, Chlorthiun, Systox phosphamidt, physostigminc, and galanthamint. 45 references. Educ. 3(1), 4-7(19G7)(Eng). A review is given of Hg P. S. Sarin ,itv, covering its history, threshold limits, mode of absorp* 20555s Neurotoxic Ride effects of certain organophosphorus .<> and distribution, and treatments for Hg poisoning. 33 compounds. W. N. Aldridge and J. M. Barnes (Med. Council 'rjf'Kti. CRJN Labs., Carshalton, Engl.), Proc. Eur. Soc. Study Drug Toxicity :.54S* Fluorocarbon toxicity and biological action. J.Wcs- 8, 102-8(19C7)(Eng). A review of delayed neurotoxic effects k sbytnn, Jr. (E. I. du l'ont dc Nemours and Co,, Wilming* of some organophosphorous anticholinesterases. 20 references. i. Ini.). Fluorine Chem. Rcc. 1(2), lD7-232(19G7)(Eng), Jenifer A. Edwards : i i extensive review summarizes the* known toxicology ol the 20556t Biochemical and physiological causes of the toxicity (c.olkanes, the fluoroalkencs, and the lluoropolyincrs, and dis- of xlcohol. Kyszard Wiklor Schramm and Hulina Schrammowa .. ics various aspects of their biol. action. Much more iu- (Univ. A. Mickicwjcza, Poznan, Poland). Piychiat. Pol. 1(3), i (atiwii is needed on the mechanism of action of these sub* 3 l3-7(l!Xi7)(Pol), A review with 47 references. Y, 1`omeranz 'vet. Understanding their mode of action in relation to their 20557u In vivo deiodination of Rose Bengal-111! in rats after constitution should be a governing factor in further ill- administration of CCL. II. llcrgnor (llumlioldt-Univ., Berlin). rations of fluorocarbon toxicity. 57 references. Acta Biol. Med. Cer. 16. 294-9(I9CG)(Ger). About double the M. M. Judge amt- of u`I-labclcd Rose Bengal was dciodinatcd in vivo in JC54W The eSect of fluorides on livestock, with particular rats intoxicated by 0.1 ml. CCL/100 g. as compared with con v'ernte to cattle. James L. Shupc and Ernest \V. Alther trols. With a protein-free diet, the effect was smaller and s Azr. Res. Scrv., Logan, Utah). Handbuch Exp. Pharma- could not be detected after G days. From CZ 1967(30), Abstr. * 20(1), 307-54(I9GG)(Kng). A review of the effects of No. 1504. MZCR *" sslnon sheep, swine, horses, turkeys, and, esp, cattle. The 20558v Effect of acute and chronic hepatitis and of fatty liver 'vis of fluorosis in cattle on teeth, bones, hair coat, skin, degeneration on erythropoiesis. B. San, S. V. Kirilina, Sh. `'tv, soft tissue, kidney, liver, reproduction, blood, placental l>an, and L. Oros. .1eta Conv. Med. Inlernae Hung., 3rd., T1'-drr, milk production, digestion, metabolism, and enzymes Budapest 1965, 923-8(Kuss). Rabbits were orally given 3 doses ***' tfisctissed. A comprehensive guide for diagnosing and of 0.25 mg. CCL/kg. and then i.m. 3 doses of 15 mg. phcnyl- '(Sailing fluorosis was given. 89 references. hydrazinc (I)/kg. Consequently, plasma enzymes (alk. phos ,, Patricia W. Heenan phatase, aldolase, glutamie-oxalacetic transaminase) increased, 150m The mammalian toxicology of organic compounds "i'j.iung fluorine. J. Wesley Clayton, Jr. Handbuch Exp. i `'wjeof, 20(1), 459-500(ll)GC>)(Eng). A review of inam- but crythrocyle enzymes did not change or slightly decreased. After a few days, serum enzymes normalized and administration of 1 did not further alter their level. At the same time, erythro 1 aa toxicology, history, and uses of fluorocarbons, including cyte enzymes increased in activity due to I and the increase was ` - vTissiun of the toxicology of fluoroalkanes, fliiorocyclo- Correlated with the no. of reticulocytes. Later, these enzymes *41 fluoroalkencs, fluoroaleohoK, a nil lluoro iroinatie normalized as well, with the execution of glucosc-fi-phosphalc *!'., their acute and chronic inhalation toxicities, acute oral, dehydrogenase and aldolase, whose increase outlasted normaliza *1 . t eye toxicities, and their biol. activities. 72 references. tion of the reticulocytes, indicating the presence of a large no, s., Patricia W. Heenan of young erythrocytes in the peripheral blood. These changes 4 `'1,n Botulism. Anton Skulberg (Fur'knitigsutvalget _ Ol'hi, Norway). .Vnrji Pehdyrbhtd 41(S), S.V.I-fil *,, *v,,rweg). A review of the subject in eonneeiion with were similar to those in erythrocyte enzymes in animals given only I without CCL; it is concluded, therefore, that a slight arute injury to the liver does not alTcel erythropoiesis. Chronic poisoning of mink in Telemark, Norway, due to injury decreases erythrocyte survival time and accelerates " '",a,,i] l>ntall mini toxin in the mink feed. erythropoiesis. Nl. Kalab - X'.ilboig A-A'liehong 2055OW Poisoning with organic mercury compounds in the * " ,0(ulism in mink. Steinar Mange, Anion Nknlbeig, Niigata prefecture aloii;; the Agano river. 1. Detection of - , rin` (Norges Yctcrinaerhocgsknle, OsUi, Norway). ! ,,'g 41(1S), 510-11( lhliT)(Nora eg). A review ( ^ 'noiict in cunnerthm with tlie recent cases of poisoning m niethylmcfcury compounds in hair of patients by gas chromatog raphy. Yukio Takizawza Sind Takao Rosaka I'ak,, (Med. Lniv, Niigata, Japan). .Ida Med. Hull. (Niigata) 14(3), 153-01 M -i 4\*1S t-f ['utruliuiii but idi a tun in Telemark and Aust- (PJG(i)(Ger). Elgin patients exhibited poisoning attributable to ., ` ''may, (lljug an aiutn.il very sensilive to C\ organomcrcury compds. Hair from tbe paiieuis was treated w Inxni, vaccination of the puppies should be recoin- with detergent, water, 11CI, CHCL, ami dithizone before anal, i " a prophv] letie niean*. Y.diiorrAseheblioyngas eliromatog. was carried out with a Slnmazu GC-1C app. i inert term chcraical danger. c,e,,r.i.. I.e .`.ioan wi;'n enctrun capture detector lECD-IA) with the conditions: ,r:i|o Pail'), fhnrnl. hr. 1007: ! A,., 1PC 3'I|,1T), column 1.3 ui.. inner diam. approx. 3 mm.; column temp. '* given of tlic hazards of e\plo-aon. p'li-wming, ele., l!IH-5, 15 or 25'; dictliylcuc glycol succinate on CU-S0 mesh ' fhe precautions that should be taken against them. Siinnaiitc; N carrier gas at 35 ml.,min.; detector temp. 2lJd; 'Kj'' .. George M. ILixrking sample size 0.5 pi. Scpn. of methyl-, ethyl-, and butyimercury .I .,_ ."aurotoxicity of anticholinesterase agents. An- chlorides was achieved with the ECD-IA detector, but not by r, |L `,<CIluf; <'! various centrally acting drugs. G. Diguami flame ionization. D. S. Plaut * v-atti (lit. Super. Sanita, Rome). I'roc. Bur. Soc. iflwrtiiiTntinn mI aubtle .toxicity f mtmw plaauc 0 $ g l" 7 4 cl OLI 5798 i 1G99 Chi'iit" el /Wiili.icli Vul. 08. 1968 7/ Pag* H i nxidn. ii( Dl'NII which n Jills fniiii ah , mi l.il>-ili .in utlitlnt-- km and III |H-rwuis who h id died fruni alllernselrrnsis and all ukidn. of fully nods, nrclylCaiA geiieiatmti, and sub j-iinntly nip-s n at ion (2 3',i. ah. m the lilood) were Mm lud lnstol. am glneinicogcmMs. J1 ulmim .. Ill J N IiisIikIhiii, An increased size and wt. of the heart caused by .> 1699a Determination of the toxicity of qocrcimrritrin, its (Simplex of |iathol. processes was noted in |>ersons with ak. aglucone, and the amount of flnvonnid* obtained from cotton intoxication. A damaged jKrinejbdil) of blood vessels and flowers. 11. K. Tuiiiytinls anil I.. A. Kl'kind (T.i'hkinlsk. sir....... edema eouneclid with the uertimiilaiion of ueid uiuen 1 (Vo:,. Millui-.t., 'Juslikriu), . .1 hi<l. ,\itnk t ch. .VVA" 2-1 |mlys.in-|iarides, pruteiii, and fatly inyocardiimi dystrophy uo. (8), ilO-H I9Ti7)(Ku's). J lie tnxieitns of (|llrll'i till 7|:llicnsnlr nliserveil. N. Mastahr i (1). its aglucone qncrcetill (11). anil II.1vonolds (111) i-xttl. from 1706a Toxicity profile* of vinyl and polyoleftnic plastic* and cotton flower (10S-F) were studied in 5 groups of (1 mice. Prcpns. their additive*. Wallace L. Guess and Sol Habcrman (Coil, were given pcrorally in 1 ml. of distil, water daily for 12 days. of ritann., Idniv. of Texas, Austin). Tech. Rap. Reg. Terh. 11 was administered in a dose of 1 g,/kg. I>nly wt., doses of I Can}., See. Plasl. Eng., N. Y. Seel. 1967(Scpt,), 15-23{Eng) and III were not given. Tile av. increase ill wt. w.is detil. l'Jastics were implantisl into rabbit muscle tissue by cutlm, Tiicn the animals wire decapitated and internal organs were slivers of plastics into scctiuns 1 mm. X 1 cm. Tiiesc slim r, studied lnstol. No morpliologic.il changes were nntrd in the were placed in a hypodermic needle and inserted into the para brain, lungs, heart, stomach, pancreas, liver, kidneys, adrenal vertebral muscle of ancsthctixed rabbit*. One week later tin glands, and gonads of animals administered I, 11, or III, except rabbits were sacrificed and the implantation sites exaind. for protein dystrophy observed in the liver and adrenal gland cortex evidence of a histopathol. tissue reaction around the plastics. gone of some cxptl. as well as control animals. F. Vitek A cell culture technique was also used (C.4 62:9072c; 63; 10545c). 1700u Effect of email concentrations of thiophene and ehloro- Exts. of plastics were prepd, by extg. for 24 lirs. in a Soxhlet isocyinates on the ascorbic acid content in rat organs. N. N. app. using 95% EtOH; the ak. was removed by gentle heat m Pushkina, 1. A. Zibircvu, and Sit. S- Khikmatiiliacva (Inst. vacuo and the residue was reconstituted with normal saline. Obshch. Kommun. Gig. im. Sysina, Moscow). Gig. Sanit. These exts. were then evaluated by mouse i.p. injection, rabbit 42(10), 103-5(19G7)(Russ). inhalation of thiophene (3 or 20 intradcfmal injection, cell culture techniques, and hemolysis mg./m.*), p-chlorophcnylisocyanatc (0.03' mg./in.'), or r- liability to a 2% suspension of washed red blood cells. Ale. chlorophciiylisocyanate (0.1 mg./in.*) by rats over an 80-day cxtns, of one of the polyvinyl chloride (PYC) resins revealed period decreased the adrenal, kidney, liver, and brain ascorbic that the supposedly pure PYC resin contained an av. of 3.5'% acid (vitamin C) levels. This decrease was accompanied by extractable material, which appeared to be a waxy-like semi dchydroascorbic acid and diketogulonic acid accumulation solid material. Some of this material was pushed through a in the liver and increased urinary excretion of 17-kcto steroids. needle into the muscle of a rabbit and gave visible necrosis and BJJK microscopic eosinopliilia after 1 week. Two different lots of 1701v An experimental study in dogs on the usefulness of PYC resin contained toxic material which was teachable into a Xnannitol, fursemide, and methyl phenidate in plienobarbiul biol. system and an extreme eosinophilic response was noted. intoxication. S. Y. Gokhalc, K. K.. Gudibanda. D. G. l'atel, A large group of chcm. agents (17 phthalatcs, 5 scbacates, ti and U. K. Siieth (Seth G. S. Med. Coll., Bombay). Indian adipates, 7 citrates, and 0 miscellaneous cotnpds.) currently J. Med. Res. 55(10), ll(J7-20(l!*(J7)(Isiig). Acute intoxication being used or having potential use in various plastics formula by plienobarbit.il (I) (100 mg./kg., i.p.) was studied in dogs. tions were investigated for toxic potential. As a group, the One hr. after 1, i.v. infusion of 20%, mannitol (11) (375 ml. in stabilizers showed the greatest degree of toxicity and if these 110-30 min.) or i.v. injection of fursemide (III) (20 mg.) in- were used in conjunction with a plasticizer in a plastics formula- creased the 1 excretion to 13.58% and 5.8',,, resp., as compared tion, the toxic potential was greatly increased due to an increased to 1.78% of the injected dose in controls. A combination of II opportunity to migrate from the plastics. M. M. Fctkovich and III did not act synergistically. II (20',)) in 3 infusions of 375 ml. interspersed with isotonic subtle (500 ml.) caused an excretion of I of 47.7%. Saline alone was less eflcetivc than II. 1707b Changes in resistance to acids of erythrocytes during poisoning by some industrial poisons. M. G. Polyak, P. A. Balander, Y. N. Fcdyanina, and T. 1.. Nevolina (Nauch.-Isslcd. Methyl phenidate, 10 mg./kg. i.v. 1, 3, and 5 lirs. after 1 in creased the urinary excretion to 5.2%, This was thought to be due to high blood pressure and hyperventilation produced by Xncthyl phenidate. 27 references. FI1JX Snnit. Inst.. Novosibirsk). Vep. Biofiz., Biekhim, Paint. EritrelsitK\ Akad. (taut SSSR, Sib. Old., Inst. Fit. 1967, 173-0 (Russ). The ellcct of mcsidinc (I), dichloroisobutyleuc (II), and dioxydiphcnylpropanc (III) on erythrocytes was tested in 1702w Toxicity of dimethyl sulfoxide (DMS0) to fish. 50 rats and 28 rabbits. After I inhalation of conens. of 1.8--1.7 "Wayne A. WilUord (Bur. of Sport Fisheries & Wildlife, I.a mg.,'1..close to the LD, the no.of erythrocytes was not affected, Crosse. Wis.). Invest. Risk. Contr. No. 20, 8 pp.(lt)li7Kling). but mcthcmoglobin increased by 3-5%; this increase, neverthe Toxicities of PMSO to rainbow trout, brook trout, lake trout, less, was not correlated with the severity of poisoning. In -carp, black bullhead, channel catfish, green sunfish, bluegill rabbits chronically poisoned with 0.01 mg. 1/1., reduced gluta and yellow perch weredetd. ill 24-, 48-, and ftli-hr. static bioassays thione in the blood increased after 4 months, whereas lower doses at 12. Toxicity was observed around 30 parts/thousand and of 1 were without effect on its level. Acid resistance of the 'was not seriously affected by water quality, although increased erythrocytes showed a left shift after poisoning with 0.001 mg. temp, increased the toxicity to rainbow trout. A preliminary I/I.; after 0.01 mg./I. shifts both to the left and to the right test indicated that DMSO has little cflect on the toxicity of occurred. II caused injury to the liver and was more toxic than -antimycin to bluegill. S- Allen CCh: 3 mg./l. caused hemolysis in rats, their erythrocyte no. 1703x Accidental organic phosphorus poisoning: the use of decreased from 8.3 to 5.8 X 10*/inm,* and Hb decreased from (propranolol to counteract vagolytic cardiac effects of atropine. 14.8 to 9.0 g. %. At the same time, reticulocytes increased from A. Valero and D. Golan (Med. l)cpt. D, Ratnbam Govt, liosp., 4fi0 to 70S X lOViiim.* Changes on crythrograms of rat.-, Haifa). Israel J. Afed. .Sri. 3(4), 5b2~4(l*Jlj7)(Eiig). The chronically intoxicated with 0.0 nig. II/l. for 3-5 weeks were shortening of the time (or coronary filling caused by the excessive similar to the changes after acute poisoning, but the no. of tachycardia resulting from atropine administration after org, 1* erythrocytes, reticulocytes, and the concti, of Hb did not differ poisoning has serious deleterious effects ml the heart in the from intact animals. Ill had effects similar to phenol; crythro- presence of hypoxia. The patient, a young healthy unman, grauis normalized within 25 days. Crystn. uf native 11 la nc- -demonstrated cleetmcardingrain ehane.es afier one day nf sums curl ed ui the erythrocytes of rats poisoned with II or III, tachycardia at 150-180 beats mm. Shortly after injection ol 5 M. Kulab 4ng, of propranolol, the electrocardiogram reverted to normal. 1708c Glucuronidc formation in esses of toxic liver damage. This proci'lure was extremely safe, eun m the presence nf heart K. Heck, U. A. Kneliii. and H. Nouraie (Med. tlniv,, Freiburg/ disease. Independent nf the sinning of the heart rate it is Itr,, tier.). A, in Urj,nt,.-S),lr,,<d. 14(5), 28<I-<)1( 111(17)`.eO thought that propranolol also has speedie ant (arrhythmic action, knldiits were poisoned either with a single s.c. injection of 1.5 'making this drug dually beueliei.il m eoiiutei.ietiue. the vagolj tic ml. CC'li'kg. of body wt.. tl..'l ml. CCh-kg. of body wt, eneh effects of atropine ami m guarding against ventricular fibrillation. 3rd day ti limes, n total of 4(1 ml. CCIt over a long period of time, Mahmoud A. layer or with daily s.c. injections of 0.4 ml. 5% aq. allyi ale. (I) solo./ 1704y Organic phosphate intoxication. Wendell I,, Fair- kg. body wt. for 23 days to test the liver capacity nf glticurouidv banks arid Kenneth C. IlnlTmati. \rh, At,Ur Mid. 7. 52-S', (II1 syntlirsis. The rise of plasma Il-glucuronic acid till) as w- " 37l'i-('T,IG7;';;ii':l. .'. d!-ch--'"i ..f 2 . : . ..( |,h o-.- , s the miliary eicntinn of III afier loading with 1 g. .Y-.-.c poisoning, eiupli.isirm-' tin- role ol elmlnu -ter i--, s in n sist.itnc p-amhiuphei'.u] showed that the max. blood levels were reach'd ami of atropine and the oxime drugs 111 treatment, 'flu n.evlia- only alter 3 lirs. (in normal animals after 1 hr.), while the total nisin of toxicity and the rationale of treatment ate detaili <1. increase was also considerably lower titan in normal aniin.d- William F. Urucc with a concomitant delayed urinary excretion of III, The dis 17OSi Histological and histochemical aspects of the morpho turbances of the If synthesis arc not as marked ill cases of sub logic alterations in the heart muscle caused by alcoholic in acute poisoning, while in chronic poisoning (CCU cirrhosis I toxication. V. 1. Yakovleva (Nauch.*Jssl-,-d. Inst. Sudclmoi only a shift of the max. to the 2nd hr. was observed. Poisoning Med., Moscow). Sudebna-Ated. Eksper'.tza, .Mm. Zdraveokht. with I produced.no significant influence on II synthesis. These SSSR 10(3), 25-30(19G7)(Rus$). Morphological alterations results confirm findings in humans in which a disturbance of U in the heart muscle of 8 persons who had died from ale. int j\iea- formation (after loading with menthol) only occurs in cases with OLI 5799 ifi 74.152 C/n iim.d Ab-.lrocl:. Vtil. 00, 19G7 hemagglutination reaction-cxtn. pmific-.ili..n i.f antigen-- Innnunochcm. ((tidies of insol. viln.n M'li . lii.n nf in i' liv.'liui nn Ill'll Il(t / |iov.i) iif.'.'/ii*. Sinn- Uuinj 724<i5r. l''lutirrstcnrc dc|>ol.iii/niii,n j,,, , t|, fiiiiinx ih.'I nn.in ji'' In' Ii"i> nl ". in uliii f( l*m l) jtyt' n< liniyiii ;n>'l Imiviih- mtiiih i 'iiijm'.ii, ., f j f|i(. 14--TOXICOLOGY T. R. TOKKlvLSGN 74452h A simple apparatus (or the estimation of some gaseous or volatile toxins. 11. 1.. lUiiu.m and Cl. Mniiv.inn (f'ac. Mill. 1`lianu., Names, !'ranee). .Inn. liwl. Clin, Il'arixj 250-2), 21fl-27(1967)(Fr). The app. is made up of 2 comp.inmenu con nected through a glass stopper. The first one, of known vol. (approx. 100 ml.) contains the sample to be analyzed. The second one (approx. 1(1 ml.) contains the reagent- used in the detn. By connecting the 2 containers, the reaction can proceed and the detn. carried out colurimetrically or vulnmcirically. With this app., CO, CO], NjOt, 11CN", and trichloroethylene were detd. within the limits of the sensitivity of the sitcctlic detn. Rene Evard 744S3j Poison chamber and * setup for creating constant vapor concentrations under dynamic conditions. X. Sh. Vol'bcrg and A. A. Goluliev (fust, Ittd. Ifyg. I'm!. Diseases, I^ningrad). Gig. 7V. I'mf. Zaliol. 10(12), 'In- -V)I HXi<i)(Russ). A chamber is described which cnutaiits small llasks fur individitat mice. The flasks arc supplied with class capillaries to ensure const, flow of poison-eonU'. gas. This app. was suggested for poisoning mice with halosilanes. To avoid halosilanes decompn. with moisture, air was dried in a column of silica gel and then on aeolitc NaA (mol. sieve), lidct of toxic fluid terminates on an eke. heated coil, where the fluid evaps. and enters the air stream. Miloslav Kalab 74454k Toxicity studies of latex rubber and aoft poly (vinyl chloride) at tubing materials. Comparison between in vitro tests and results of prolonged administration to rats. L. H. Eklund, C. A- Grant, and V. Willncrs (Kg). Farm. Inst., Stockholm). . Acfo Pharm. Sutrira 2(5), 349-5G(19G5)(Eng). A comparison lias been made between in vitro and in vivo proper ties of water exts. of latex and poly(vinyl chloride) products. Sixty rats were injected 1 tnl./lOO g. of body wt. i.p. for 12 weeks. Hematological, liver and kidney tests, and pathol. cxamtis. were carried out. At the end of the study, no appreci able differences from the control animals were observed. The value of in vitro tests as a relevant parameter of toxicity of polymer products is discussed. KCTT 74455m Alterations in microsomal electron transport, oxida tive N-demethylation, and azo-dye cleavage in carbon tetra chloride and dimethylnitrosamine-induccd liver injury. E. A. Smuckler, E. Arrhenius, and T. Hultin (Wenncr-Gren Inst. Exptl. Biol., Stockholm). Biochtm. J. 103(1), 55-C4(19G7) (Eng). The effect of administration of CC1, and dimethyl- nitrosamiuc in vivo on hepatic microsomal function related to drug metabolism was measured. The capacity of isolated rnicro- aomes to dcmcthylate dimclhylanilinc was diminished during the 1st hr. after CCh poisoning and during the 2nd hr. after dimethyl- nitrosaminc poisoning. Thereafter the microsomes from CCh- poisoned livers showed a continuous decline in activity so that at 24 hr*, there was little residual capacity to undertake dcmethyla- tion. Microsomes from dimcthylnitrosaminc-poisoncd animals were not different from controls at 24 hrs. During the rirst 3 hrs. there was a transient rise in the accumulation of the A'-oside intermediate in CCh-poisoncd livers, with a subsequent fall to below control values. In dimcthylnitrosaminc poisoning there was a parallel decrease in jV-oxidc accumulation with decreased deiuethylatiiMi. In the latter part of the first 21 hrs., thcratioof A'-uxidc accumulation to (leint thylalion was increased in both instances. At 2 hrs. after poisoning with either compd., there was no evidence of altered XADI'fl-depeiuleiit ueotclrazi/liiim reda. or lipid peroxidn, XAlil'lI-depoudeut azo-dye cleavage was decreased. There was no difference in microsomal cyto chrome b5 content, but there was a decrease in the amt. of cyto chrome }'-45fl. This latter ciiangc was correlated with the decreased capacity for NADPH-depcndeiit oxidative demcthyla- tion. It is suggested that dimetiiylnurosnmine is assoed. with a defect in microsomal NADPH-dcpcmlcnt electron transport at the level of cytochrome P-4.VI. In ndrin, to affecting cytochrome P-laii, CC1' is assoed. with a Uni! -t.Vcre block involving the rcku-e of fon.iuhlLhydc from ike A-oXale mu'nu tii ile. KCI'G 74456n The effect of the aflatoxins Bi, Gi, and G; on protein and nucleic acid synthesis in rat liver. Janet 1. Clifford, K R. Rees, and M. Elizabeth M, Stevens tL'mv. Coll, llosp. Med. School, London). Biochrm. J. 103, 23M~G!t ll)ri7)(Kng). A comparison lias been made of the difference spectra obtained by causing x-arious allatoxins (Hi, Co, ami CL) to interact with calf thymus DXA, The effect of these toxins on RNA and protein l synthesis by rat liver slices lias been measured. The extent of their inhibitory action on the synthetic n actions war proportional * " 11 - f.(' oi i > .ii , I,. ` -s ` i..r , ', wiih DNA. It is proposed that their toxicity depends . action. It was demonstrated that the K\'.\ nucleoli isolated from the livers of ullaioxiu !!,-[o>i,, inhibited. This finding is in agreement with t!. mechanism for the hepaioioxic action of aflatoxin. 74457p Effect of pretraatment with polycyclic k . .on the meUbolitm of dimethylbenzantbraccncir.'L .- and other tisaues. 1'. II. Jellinck and liarlnra , British Cohimhia, Vancouver, Can.), Btoihctr, 1611), 131-41(19G7)(Eng). Pretreatment of ruts v polyeylic hydrocarbons (3-mcthylcholanthrcuc, anthracene, ben*o(o)pyrene, anthracene, phen.mr . naphthalene) alters the metabolism of 7,12-dinn; anthracene (DMBA) by hepatic tissue from sidc-v! hydroxylatiou. No change in the metabolism of )>;,!. adrenal glands was oliserved under these condition , liydroxylated metalmlite of the carcinogen v;is [.mis tissue. It is suggested that protection by aromatic by1 against DMBA-induced adrenal necrosis is achieved In . the yield of the 7-hydroxymctbyl deriv. of DMBA in This product, rather than the unchanged carcinogen, ; the proximal necrotic agent by virtue of its structural t. to the adrenocortical steroids. The cytotoxic cff. . adrenals may be due to damage of cellular mcu.ktelease of lysosomal eniymes, 24 references. 74458q Metabolism of chloroethanol in the rat. Johnson (Med. Res. Council Labs., Carshalton, b:; chem. Pharmacol. 16(1). 185-99(19G7)(Eng). ttT. ethanol is given orally to rats, liver GSH (reduced is rapidly depleted and 5'-(carboxymethyl)glutathion< Release of **C1- from chloroethanol-**Cl has been stinlw and shown to require stoichiometric amts, of GSII tl NAD (2 moles), A'-(Carboxymethyl)glutatliione < identified as the product in vitro. Ethanol inhibits iN of GSH in vivo and release of MC1_ in vitro. Chlur. readily dehydrogenated in vitro by purified yeast an*: ale. dehydrogenases. The route from cldoroelh.ui"! boxyinetliylk'lutatliione has been studied in vitro. methyl )glutathione is degraded by kidney liomoge'iiate : glutamic acid, and S-(carboxymethyl)cysttinc. he metabolism of the latter compd. is discussed. It i- that the toxicity of chloroethanol is due to its cote, chloroacctaldehyde in vivo. 74459r The effect of carbon tetrachloride on rat i Comes. David H. Alpcrs and Kurt J. Uselb.iclnr Med. School, Boston, Mass.). Biochim. Biophyi- - 33--12(10G7)(Eng). The effects of CC1, on isolated and rat liver slices were examd. The addn. of CCh ' lysosomes caused the release of ff-Klucuroniclusc, ae:. tasc, and acid RXasc activity. The release occurro' Jag period and was linear. In addn,, the rate of : dependent on the C.CU conen. CCh added to hycr so a redistribution of the lysosomal enzyme activity -ti greater percent was found in the supernatant vs. the 1 fraction. Under these conditions leucine-`*C incorr protein was inhibited. The effects on lysosomal enzx leiieme inoorpoiatiou were roughly comparable fur a - 1 of CCI,. Studies of the kinetics of these changes n to he linear and to occur without any deieciubl' Lyso-omes were isolated by 2 different melluids, so . peroxidn, occurred to a muck greater extent in one 1 pared with the other. Despite tins difference, Cx. comparable release of lysosomal enzyme activity in Furthermore, in neither lysosomal fraction did Ct lipiil peroxidn. at a tinm when its effect on enzyme max. 32 references. 74460j Veterinary toxicology, to make a diagnose Buck and Virginia Mar-hall (Iowa State t'niv,, S:,i!- L'nh-. Va. 28T7-f>(I'ubk i I'n-r'. N-m'- cliem. toxicants and their diagnosis in vetvre. irx discussed. Mm'. 74461k Histochemieal enzyme levels in expe:. '- cirrhosis. T. Ta-liev, I,. Kruxtev, and L. B.ila Insl. Khriintiir. Bulbar. A had. -Vuint 5, 2k x- 2 Uvptl. hver ciirlmsis was induced in rats by dailv injection of CCh fO.On ml.) during 3 tuontlK. Aik. i was ncg. in normal liver parenchyma and bile dir' strongly pos. m hepatic cells of cirrhotic areas, changes were oliserved xvitli acid phosphata-c; it- 1 rii-ernssed in half of the exptl. animals witli liver en' OLI 5800 Vit! lilt, I'M*/ P, |* ,mloj*y ' Ii.mi, 'ihlOIII- UlllillU There but oology lotions li.ition JMH (ion 12. i'JSOIIK* t. Dif61944V. duitary .net in 62210q. Iiininlii.iMii.tioil'lll I* *., Iiilt.tn it I'.il.'itiilllii III t .`i'll . i*t 1*1.' .111*1 16y l. till (ltn.vil.il 11 til|70y. Ililliu nil llM-11 .111*1 .................. cX|iivsxioii of |*nlcnti:il :ntiiiuxl>>mlm*im: vll. m |ii* v ii.-. *,| rli|*ir.iiii|i)i*-iiii`") (Sclim-nlicri:) tflOlOy. Ai'ti*ili **f ln'iiini :m.l iiiiiiti'igmiuidim* on au-niliylm-liv. ;iii.i|iliyl.ii*iv|ii. -n*t In .l.iniin*-. imliiivil sliiH'k in Kilim .i pii-.x |t'.ii*il// 64i7Rj. I'.lfi ii i*f mil en.iKiil.iiii v on iWV.iyi'il ti v)h-i vn'itivity I * -III I. *'I It nti*'ii) (.tit'll. Siilc effects of drug, on gr.inulo|>uK-sis ami llnnmli*i|i*ii> m, (Hoppe) 639J2g. Inhibition of eiiloroi>!iyllin il.nvs, ugjin,i complement activities anil anaphylactic reaction (Sindo) 04140r. Effect of X'a Cu chlnropltylliii as cinntilciucnt infiiliitor mi allngraft reaction (Fujii) 64141s. Effect of liiiunm lnz.it liMiptiue! on susceptibility of guinea pies lo allergic encephalomyelitis (Field > 6406411. Elucidation of structure of Yi-auligcu isolated front (Esrluiichia coli) 539G/38 (lieynsj 05785s. Effect of chloroprcne on immunologic reactivity of organism in |iervms vaccinated against typhoid fever (Mikaclyan) 5&658I. Analysis of the crystal antigens of Bacillus thuriiigicnsis by gel diffusion (Pendleton) 62794h, Interferon and intcri'cron-like substances-- present state of usearch (I-ackoyic) 02728q j'atrn!: Allergen prcjins. (Aktiebol.ii; Ccrncllt) 588451). --TOXICOLOGY t. a. roaxsLsoK i logy to pounds; faraeillc, i.<nwuu., \ review roperties . Colas t water. I). Car, present r babies, bacteria itiont of bstances. Mizengart lr. Prof. original ylaminc, titan on ture and ior hypoextent of reported. Kalab . vaminaJ. Nutr. A review the signs principles tria were The chief d other available " carboxy .ivs. have ithyrism aching in .micron ilium B. * Ames), tiosis and :' arc disacobson 'os (Texas n. 18(4), poisonous h*s, fungiXumerous Voii eipos-i^^alcohol ^Bid ^Jcicand. bong-term Hisin and .ehtmdrial metabolism "wi'ignifi alight in- crease in that of neutral lipids were observed in mitochondria from alc.-fcd rats, compared with controls. The compn. of the phospholipid fraction was nearly identical in the 2 groups of animals. 22 references. BXJN 63866v Diuretic therapy of acute intoxication with hypnotics. G. A. Krueger (Evangelischcn Krankcuhausct, Muclhcim, Ger.). Anaesthetist 16(2), 40-4(1967)(Ger). furosemide (20 ntg-), injected i.v. into patients with barbiturate intoxication and added to running infusions dependent on the progress of the ease (an av. of 20 mg /lOfib ml.), was an cflective therapeutic measure against the intoxication. The drug '.is easily ad ministered and could lie safely used in case of diabetes or com plications caused by depression of cardiac, circulatory, or liver functions. It considerably reduced the time of unconsciousness and hospital treatment. Circulatory analeptics, particularly cthyldiphcnylpropcnaminc, were effectively used in cases of hypotension in order to reestablish normal blood pressure values. 46 references. BKJG 638G7w Electroencephalographit changes in chronic poisoning with trichloroethylene. K. Schunrizova f Karlova L'niv., Plzen, Czech.). Cent. Neurol. 29(C), 369-77119ii(i)(Czcch). Exoinns, of 78 persons, exposed for 7,5 years mi the av., re vealed insufficient mental relaxation, lowered vigility, amt dis turbance of the a rhythm (on tile border of abnormality) in 40.1%, small focal lesions and few synchronous 0 waves Might abnormality) in 5.1%, and frequent disperse or diffuse 8 waves with synchronous exacerbations or focally accentuated (moderate abnormality) in 34.5',,', of the cases. 1.. J. L'rbamk 63868x Depression of potential myocardial contractility accompanying chronic ethyl alcohol administration. Julia Elwood Maincs, III (Tulane I niv., New Orleans, l.a.), Ttie. Microfilms (Ann Arbor, Mich.), Order No. 66-10,767, RX pp.; Diss. Abstr. B 27(5), 1501-2(19<>0)(Eiig). SNDC 63869y Subacute toxicity of ether extracts of PVC. S. Homrowski, H. Pickacz, and H, Mazur (Staatlichcs Inst. Hyg., Warsaw). Ernochrungsforschung 11(3), 398-402(1966) (Ger). Toxicity assessments of H-O-Trec EiO-0\td. plates of a poly(vinyl chloride) (TVC) plastic (consisting of l'VC 80.5, l'ala- tinol AH (dioctyl phthalatc) as plasticizer 7, Advastab 17.11 ($-contg. org. dibutyl Sn conipd.) as stabilizer 1.0, Advaw.ix 360 as lubricant 0.5, and TiO, as pigment 2.0',) were carried out by thin-layer chromatography of blood specimens obtained periodically from Wistar rats of both sexes with starting wts, of 100-125 g. In addn. to a standard diet, by means of a stomach tube, GO animals received 1 or 100 mg. PVC ext./kg. body wl./ day as a 0.3 or 30.0' suspension, re*.p., in olive oil, lor 3 month', and 10 of these animals received 1 g. undild. PVC ext./kg. body wt./day throughout the 4tli month. All exptl. animals exhibited normal behavior, appearance, and eating habits; body wt. gain' and blood-constituent values were similar to those of olive oil- treated control animals. No significant macro- or microscopic lesions of liver, spleen, kidneys, or stomach w-crc revealed follow ing removal after sacrifice of annuals by I't-.O nareo-i', v. it!) the < viepiimi **i a >t.oi .tic.i.ty -i i.nV.mt o'.*r **,1*: ,, < ir m 2S'heavier than for controls) among anm,.d* luvivj-.g * do-es of ext. Only about 23' r of the total content of non-;' ' el- contg. plastic constituents wasextd. by the Et;G, of which t"1' < was plasticizer and 3'.',. stabilizer; it was assumed that tlm othet 7% consisted of the lubricant, since the pigment is practically insol. in EtiO. On the basis of reports, the plasticizer and lunri- ctmt, both with an LDw range of 33-35 g./kg. body w t,, were practically nonpoisonous, whereas the I-D value for the stabil izer was 500-60U mg./kg. body wt., indicating that any toxicit) h / c` in |lu - M v r*lv line to llr ftltilijli/rr * i( )i|) null !<** nit:- l`V4' hi., hJi}) in Mlad ;s and 3<i mg. Mabilm-i/k.-,. I***ly wt,. li sp., did not , lu u any advviK reactions; the heavier wl. of the liver, ns a result of In ...... .. of its l>)*x) vesa-K, was ronsidi red to lie eviih-nre i,f an ciihaiici-d m-livity of this organ in handling tile increased ami id rst. content, hoy Solkot 63870s llepatotropic action of N inetiiylformauiide. v. ,\. Vasil'eva and T. M. Sukhnrcvskoya (Just. jnd. Hyg, Prof! Diseases, Moscow). Tg. Tr. Prot. Zabol. 10(12), 53-4(J9Cr,) (Kuxs). ^ A ease history; U presented of a person who drank 50 tub of A'-incthyllormaiuidc: even after washing the stomach with water, acute injury ta the liver developed, accompanied bv proconvertin (1) decrease (by 24%) in the blood and increase of plasma fibrinogen lo 010 ntg. %. I normalized more slowly tlun any other hioclicm. index. Miloslav Kal.di 6387H Toxicity of phthalodinitrile and UUacltlorophUtalodi- aitrile. I. Acute toxicity in nice. Hiroshi Yoshikawa and Kiynyuki Kawai (Nat. Inst. 2nd. Health, Kawasaki). Ind. Ilrelth (Kawasaki, Jajian) 4(1-2), U-15flDGOHKng). f ive to 3n min. after intratierilotical, subeutancuus, or oral administra tion of o-phtlmlodinttrilc (I), mice had generalized convulsion, lasting 10-16 sec. The convulsive attacks were repeated several times with 30-60 sec. intervals and death occurred within 5 lir>. Upon administration of the meta isomer of I, convulsions were less marked and animals receiving the para isomer showed only weak ness. The resp. LDm valuesof -, m-, and p-I were 34.5,481.3 and OeS.O mg./kg. LDh values for w-f and p-tetrachlorophthalodinitrile administered intrapcritoneally were 6G.4, 2.5, and 1581 mg./kg. Convulsions were absent with the chlorinated dcrivs. Emanuel Kaplan 63872u Hepatotoxicity of a series of organotin esters. David J. Galley, W. E. Guess, and J. Autian (Univ, of Texas, Austin). J. Pham. Set. 56(2), 240-3(19G7)(Eng). Four organotin esters having use or potential use in the formulation of medically used plastics were evaluated for their toxic effects on the liver follow ing oral administration. The liver damage is apparently the cumulative type, requiring several days to manifest damage in the form of elevated scrum glutamic-pyruvic transaminase values and prolonged hcxobarbilal narcosis. The toxic potential was, in general, soly. related. RCYG 63873v Effect of Vandid on cardiac functions in experimental trichloroethylene poisoning. A. Kubacki, A. Mrozikiewicz, A. Skubiszynska, and A. Wachowiak (Akad. Med., Poznan, Poland). Mod. Pracy 17(3), 19G-200(I9CC)(rol). Electro- cardiograph curves were surveyed in rabbits exptl. poisoned with trichloroethylene. Administration of Vandid (A'.A-dicthylvanillamide) (5 mg./kg.) produced no arrhythmia symptoms, which occurred, however, when adrenaline (0.1 mg./kg.) was used as the cardiac stimulant. Helena Lange 63874w Histochemical evaluation of liver extracts in prophy laxis of experimental carbon tetrachloride poisoning. Kazimicrz Zajusz and Marck Zacharewicz (Inst. Med. Pracy, Zabrze, Poland). Med. Pracy 17(4), 317-28(19G6)(I'ol). CC1. ad ministered by stomach tube to rats (O.C ml./animal) caused an initial increase of the liver acid and alk. phosphatases and ATPasc activities, but this trend soon discontinued and the enzymes became inhibited almost completely. Liver succinic dehydro genase, phosphorylasc, and the brandling enzyme svcrc also totally inhibited. Enhanced reactions for alk. and acid phos phatases were observed in the kidneys of the poisoned animals. The effects of CC1, were markedly moderated by prophylactic administration of hepatic exts. Helena Lange 63875* Pathomorphologic changes in white rat organs during chronic combined inhalation of methanol, aqueous ethanol, and furfural. R. U. Ubnidullacv and P, V. Panov. Med, Zh. U:b 1966(9), 70-3(Russ). Three different eonens. or a mixt. of vapors of MeOH, aq. EtOH, and furfural were used in an in halation expt. of 3-mouths duration. Severe histol. changes wore found at the highest conen. only (5.79 mg. MeOH/m.J28.48 mg. EtOH/m.*-0.3 mg. furfural/m.). RNA of bran, and glycogen of liver decreased, accompanied by fatty livn di*.trophy, J. IVokcs 63S76y Morphological changes in the organs of animals in cute and chronic intoxications with a-mcthylstyrene and styrene ' 3. Veselova and G. A. Ogleznev. .Xciuh. Tr. Omsk. M 'd lost. N'o. 61, 89-95(19C5)(Russ). Expis, were conducted m. 'lice and rats administered intrngastrjeally an aq. soln. of u-mdl Hxlyrcne (I) or styrene (II). Internal administration of mux tolerance doses of I (3 for mice and 4 g./kg. for rats) and II 5 and 2 e./kc.. resp.) caused no marked morphological cu.m aiilc I intoxication-., grave licuiod; uamic .uni 1 j -tr ; ' mges in the parenchymatous organs, most pronounced in U|igs, were recorded. The group of morphol. changes immu i lln- central nervous system of animals with I intoxication yndromc of toxic encephalopathy. Morphol. changes cae - VI intoxication did not essentially differ from II-causcd chaugi' Lhronic administration of II (0.014 mg./kg.) to rats caused d> elopmcnt of dystrophic changes in the central nervous sysi* more often than did 0.5 mg. I/kg- under the same condition.. OLI 5801 t'li 11 pi'""- .ill-ill (Pill' l.V nil ll'li ilhiriiri- nf w i-rr itic.ni .ciiir tn llii-i , WITI- cniimill clili>rn.irtivilii-s nf -U'.-ic Ir.msml FrauLi-l :, vski units 1.1.1*1, liver, itiiinnls. In nua! tissues itsiik-en tlic tnzyuiic c- -roiin-lie re* liichcr level if pyridoxal tluit the in* its reaction I'.iilisliinn holeitcrol in : and bepato* i-iki-Kr;ink- tl'J), 7JH-M) . 1 -. of cliolcs* pistratioii of nm of cthioilir.iil follow* ./k.) riven CMJG rat) toxicity D. E. :t Ind. Biol. fltirol. 4(4), simlics have JhylTM*! Elyboth given TMlPt. The 1>DGB was "1-day study it. and 2.5% 'potli sexes at a as atttihut- h this effect rmatoiogical d 2.S% dictmd the rela* -reused. No I to DDGB. t.ary level of ys could Dot ted. HCTT s. Norman erck Chem. . Chcm. Six. reacts with 'ni relatively reported in- explaincd in . picxinr and RCJC 'ing agents. *111. Pharma' p>f effectivemustard, LI'riiliiccd a d iutraeere1 v included a pi of central ie behavior, tonic cxlcn' .tiniile, and I in doses of -Iiytoin fion i-ffteli ii|. h.irlnt.ina V*1 <* ./ fitine the CMJN ni-tit on the Jj. Meyers, Greenfield, '(iing). A |,ll (l|i*l lld.ll* l f I' I ' .1 l.lll I'G 1*1 \ .lift' III |H "!( t Ml |)|t * I'l* . I . gif flu tii'ii lit it nit ut tt pit p ^ i`li< ( In i ,i pi; 11 . mi l Im anil t I*n It y *( 4 ( ll'-t II l> tllffli.il .H',* lit . I . <l( . I ill' tl lit till )< i li*> <1 l>\ tliU imllii'il Ihil n`iitiip!\Im* . hi * .liniipl vln* . h liinndtin tlv if n*-t tt it Ih.'I ilt .i . .n! n .m ,*lhli\> iiiamic'. Hot) of tlf ;itilti|t pii '"Hivf rtnnjHl-. tniiladly pipi.li. jitiil the nf phyMH.tigminc and l*.. Ic-m i iltiptf |>ih*eu- ftiur. Jiphedune toxicity was sighd'aMiiUy antagoniz'd b) lliyiiioli-ptic pritiviilmciit. Tin* In verify rc|ots tli.it flic tricyclic untidepic-.'ovcs dangerously >:ii tin- toxicity of ale. or iitnii'ktnniK oxidate inhibit..ts, Ui-4ihs indicated ili.il a variety of medicinal agent* can In* tixi'd in Ilr* tinrtiiptyliiiv treated patient without any problem of tigntfscuM firing im t r action. RC\C* 1236r Chlorinated anilines and their sanitary-tovicologitAl characteristics. Cl. 1). Khamuev, Aknu. hiltory lAnWiw. Srtdy i ikh Cr^icn. Ztuirhntit, Sh.t Mrsrmv 1965, H>K lOfKti'vv;. Monochlorcamlinc is usmI in the production of insecticide* and dyes. iM-Monochloroanilinc (I)and /Miionochloruaniliiic rll; dis solve in HiO \b g./l.)p in which they cause an unpleasant laMc and odor. The odor and taste perception thresholds were 2.0 and 7.2 fori and 1.6 and 3-G mx./l. for II, resp. In a concn. of 150 mg./!., I and II lowered the B.O.I). of water. Threshold conens. arc 1.5 mg./I. for I and 0,75 mg./l. for II. The L.lJ.u values (stomach administration) for I and II, reap., were IBM and 401 for white mice, 1104 and 308 for white rats, and 760 and 350 ing./kg. fur guinea pigs. A 3-innnth Mih-arute evpt., conducted <m white mis with stomach admini-tiation nf 0.1 L.U.ii levels, caused l lit* formation nf met hemoglobin and re duced the hemoglobin level and the erythrocyte count. From Rrf.Zk.tKhhi1966IS), Pt. II, Abstr. \o.HUM. MVRK I237y Toxicity of thioacetamide. Z. Hrulxiii, W, Gradinnn, A. Slcser, and M. Lubran fUtkiv. of Chic.igu)- /wirsf. 15 (11), 174K-f#fii iwOdKIim;)' Thioacetamide (I). f*'d to rats in a diet contg. 5b mg./kg. body wi./day fur 5 days, produced high serum lactic dehydrogenase levels and ecntrolobnlar necrosis of the livers within 24 hrs.; the enzyme levels decreased and the necrotic areas were resorbed within 3 days of feeding the diet. Severe degenerative changes in the kidneys, hematuria, and in creased serum urea N and scrum creatinine K*vek occurred within 48 hrs. of treatment. The lethal efTects of the above level of I were correlated with the renal damage. Kxccss dietary casein hydrolyzatc, methionine, or guanosiue reduced tho mortality and renal toxicity of I, although these cnmpds. did not prevent the nuclear and nucleolar enlargement of hepatic cells and of the cells of the proximal convoluted tubules of the kidney occurring in treated rats. 07 references. UBJN 1238f Poisoning by grass. C. II. Gallagher, J. H. Koch, and H. Hoffmann (Univ. Sydney). .Vrsi* .Yrtrnfis/ 3l(5W), 41214(19dC)(ng). Acute and chronic neuromuscular disorders occur in sheep feeding on the pasture grass Phalaris iithernsa. This grass contained 0.3rr (dry wt.) tryptaminc alkaloids. Tissues from sheep undergoing acute poisoning showed no histol. alterations, whereas the brain and kidneys nf chronically poisoned animals showed deposits of green pigment. ( The pigment was .noted in the mitochondria cells of the mid-bruin, brain stem, and spinal cord. It is suggested that these changes are related to the oxidative deamination of .VfaV-dimcthyHrypuniine and .Vine'thoxy-ArN-difnclhyhryptaminc. The protective action of Co against the chronic form of the disease, rejHirted by others, may be related to the prevention of degenerative changes in nerve tissue or to the acceleration of alkaloid metabolism. \V. L. Downs *1239p Vinyl chloride; industrial toxicologic aspects. 1. Grigorescu and Gh Tuba. Rev. Chtm. (Bucharest) 17(S), 491* ;501(19flfi)(Koni). A hypothesis was j>ut forward, claiming that CHi:CHCl (I) could react with JI-O at the U-vd of the hepatic cell, yielding ethylene nionochlorohydrin. which could be oxi dized to ddoral and chloroaectie acid (II). II could be elimi nated as such in the urine or be metabolized further through atm`nntiou to glycocol. An anal, method was developed for detec- 'tion of II ill urine, assuming that the only ollut sonic*1 H could be massive ingestion of v ine yeasi or inlulalion of trichloro ethylene. An aliquot I2*HI cc.) of urine, acnblied with f HjSO, (2 cc*) is rad, with Kt.-O (200 cc.), shaking vigorously, and settling for 21 hr>. The ext. is drud i.mhyd. Na.S'JH. Cvajid. t*i dryness liinkr reduced pressure, and the residue is drSolved in Ah', aq. ale. sola, i'll..*) cc.)* One dr**p of the s-hii. (25-30 4*1.) is placed on Whatman No. 1 paper strips (25 X 3 cm.), dried, and chromatographed by ascending method, using as elutnnt the mi\t. NThOH-KtOH-H/* (l:2`i 4' for : fieriofl of li hr-. The sum-, drnd ir. it, ait ki pt 2) la- . i coned. N'll. ,:m.. i ,r A u\t" ..V ' ' , ; i. ninhydrm in M* OH, ami drud. Tih II is nwiiva; dby:.1 *"* violet spots. Pijr distinct flev<4opment. th>' ^trip- art -p" >d filially wall l*1' . C'M NO.): fc.irmiii'' i< d sp, ,i -1. 1 lie A' at 2*' was estabh-hid with a sola, of 2(> II/ce., as O.Sn. 1 I'* limit of >cnsiii\ ity is. 0.1 ^c. II, and is improved by the u >e of Cu- (K0|)s. The extu. of II from urine w..s th moiisti.ited by in at- ing a sola, of 25 ^g. II/cc. in mine as above, cutting tiie rori'.- ; t j > t | -j /, 1 ............ . . it spoodoi'* s|h*i-.f flulmt* the H Willi l-.lOll, nnd ilelf.. C'llornn- ti .til \ |li*vln yi* Id w.i*. - *a'jf . IVlimiirov !*, Ito II iii rim. b' .ihby fM i Jinin I, whilr .iMioiig liie sl.ifl of ] , i .`-iiit* pl.iol' , Ml', of tin- ^imphd |H`fju`- ga'e .i | m is, n.iMi'. to lb* mtlii'xl. IvxtcuMve tests showed that most of the p., teaelioiis weie obtaimsl with Staff employed 2-5 years in th plants. In thesi* eaM*s the proteinograins were inoiliiied, tin ,. l.hilmlin fi.ielion Ining higher and the vtdnhuliu fr.uin,, bring luwii than in the |KTsons with ueg. react ions to tin* pn eiice of JI in the mine. It was concluded that the oip.icity ,.j the organism to nielalioH/.e II decreased after 2 years. M. Ben Klieser 1240g Effect of hexachloro-p-xylcne ingestion on the oxidative phosphorylation of rat liver mitochondria. Hsia-Ying Chan, and Chcn-'J o Yuan (Sinn-Sovi<*t Friendship Hosp., lYkm/. China). .V/rciig H' Jfua Hiuek Yu Skcnjt I I'm Mu L% I/such /'m. 6f3)# 273-5(ll*0(i)(Ch), Oral administration of hcxachluro-f xylene (I, 0.6 g./kg./day) to nits uncoupled the oxidative ph.,-- phorylation of the livtY roiiodKnidtia, in extent proportional to the duration of I treatment. The decrease in the production o: ATP with inauflicicnt energy npply of tissue may be the of the toxic reactions of I such ns generalized weakness, fatigue, dizziness, headache. BHJJ I241q Adrenaline-buctivatioii capacity of the normal and of the CClrpoisoned Ifrar perfused in vitro. Emma Costincr, 1, Vaislvr, and Yi*jricn Cbivu (Acad. Rep. 5oc., Romania, )hi rharrst). Stuttii Crnrt/tri Awifivviwi*/. 17(1), 365 7( 1`.bd)( U.un' Noimnl ral hvtrs, nnd livers originating from CCb-tivaUii i.p wire |K`rfuM-d with adrenaline in vilru. The latter slimn-d .* lower rate of adrenaline degradation as compared with the former .. BTJQ 1242x Pyruvic acid content in acute barbiturate poisoning H. K, Muraslmv (S. M. Kirov Mil. Med. Acad., Lmiiigrad Ter. Arkh. 38(Jb), nK4~4{l`.H)b)(kuss). In d(*ep ewiu <lm t<. harbituratc intoxication, 1.2 rng. V< pyruvic acid (I) was found in liter blood, its concn..decreased with recovery to 0.77 mg. ' e When the 2 concn. rcachetl 1.8-2 mg, Vc* complications occurred and the respiration was disturbed. The 1 concn. was direct);, proportional to the severity of intoxication, as observed in a iota! of 32 ikunoikmI hunuiii.. Miloslav Kalab 1243c Inhibition of biosynthesis of protein and nucleic acids by phenolic compounds in vivo. G. V. Kukushkina, I,. B. Gor bacheva, and N. M. Emanuel (Inst. Chem. Pliys., Moscow). Vvpr, Mrd. Khm. 12(5), 452-6(l9GG)(Russ). Mice with the Ehrlich ascites carcinoma or solid hepatoma XXII were injected with a tmxt. of uniformly HC-labeled L-amino acids (I) (10 >ic./ mouse), Na formatc-uC (II) (5 *ic.) or adeuiic-^-l4C (III) (17 #<c.). After 30 min., one group .was injected mtrapemnuculiy with I*r gallate (IV) in 0.9% XaCl and another, with 4-metliyl- 2iG-di*/i'r/-butylphruol (V) in 3% aq, Twetn-SO, Controls weri injected with theresp. solvents. Ascitic fluid samples were taken from mice with Ehrlich tumors at time intervals from 0 to ISO min. and the cells washed with a 5:4:1 inixt. of 0.9% NaC), 0*3 A/ NajHBO-i, and 0.3 A/ KHiPCV Mice with solid tumors were sacrificed after 120 min* and the tumors, liver, kidneys, ami spleen were removed and homogenized. When I was used, the cells were treated with cold 5% CljCCOOH and the pptd. pro teins isolated and examd. When II and III were used, 5% Cb- CC001I washings were extd. with EtiO, the aq. layer evapd., and the resirlue (acid-sol. fraction) examd. for radioactivity. The acid-insol. fraction w'ai> washed with cold 90% EtOH ami heated for 10 mm, at 50* with EtOH-EtjO (2:1) to remove lipids. A sample was examd. for radioactivity and the rest extd. with 10% NaCl (pH 7.4-7.0) for 30 mm. at 95. Nucleic acids were pptd. by adding 3 vols. of cold 0G%; EtOlI and washed with 7(J',( EtOH. In mice witii ascites tumors, injection of 75 pig./ kg. of V decreased I incorporation into protein by 30% as com pared with the controls; 200 mg./kg. of V inhibited I incorpora tion almost completely. Injection of 100 mg. of V/kg. de creased III incorporation into nucleic acids by 20%; 200 mg. ol V/kg. inhibited III incorporation ahm^t completely, luiei tiuii nf so mg. of IV/kg. or of 120 mg. of V/hg. after 1A0 mm. *1* cleaned 11 incorporation into acid-iiisol. fraction by 43-A.V , . into nuel* ic acid by 64-01/,, into acid-sol, fraction by 50-77',. Md'into prutt ms, by 30 -14% . In mice with solid hepatoma, m* PTtion of | An mg. of lV/kg. after I AO min. decreased I tncorpoi.i t'pu into tumor proteins by 21'*', : 200 mg. of IV/kg. decre.i-'' -1 I ineoiporatioti by 03', . Injection of 150 200 mg./kg, of IV had in> effect un protein biosynthesis in kidneys and the livu normal mice and in kidneys of tumor-bearing mice which showed ""'IK activation of I incorporation in the liver. Itijiciwii of 'f'1 *'f IV d:,T. <hereaMi| I incorni-ration in\it ".ydeeg pr.iten - "d jod luni'H-bearing mn'e by 30',: loO mg./k.'. Iu*. -* l on pr.'Uin biusyntluM". in tin spleen. l\!i\ huro. 1244n Expcrmicnul intoxication by ammonium salts, pr^ h etnm by some amino acids and their mechanism of action. 1 l-nnnio and F. Sdvatore (tbiiv. N'ajiles). Hwrkim. .lp//. I-l '-> 7>7 S5(l`MUI)(Ital). The biochem. conversion of Nib m%* l,U l is dincussed relative to the protection afforded in acute .m i I, 1,1 vine XHi intoxication by some compile, nssoed. with the cun OLI 5802