Document rYLEvQ9794a730MpN6V5gY8a

FILE NAME: Chemical Abstracts (CHAB) DATE: 1964 DOC#: CHAB044 OCUMENT DESCRIPTION: Abstract Originally Published in 1963 by Davis conens. w - increased " ;te n t' irresp^ contrast to' " 15 slelv ' } f f ***** ' Snfce oh,l:vdorfPLe/r' sslbi.y e li c it CfV r a> V Ackerson ' "itoxicatioaj Malloy, a,,^ ngton, D.C \ -), infused as ' ,a t 5 Ml./mia urine outpilt 'ith moderatj 'onic bromide cute uric acid tons diseases a hemolytic treated with I and shorter tients with H iromidism, J 1 a nd salt di'ia, azotemia, a (e -g- by M its suggested velopment of ,ma and that eatm ent may eeommended nts with ma n s . After a ed promptly om Peskm 5. Jr. (U.S. 19(3). 20-2, \ Chichilo aoxon. VI. mal passage. J. Invest. the cat the wing topical K 10~*mole/ hrs. corre ma cholinesaoxon, inditer does not opically aptefore it was . Jackson phosphoric es). Igiene The role of nimals and four sisters aption of a Symptoms rs. Death is but post ed this not presence of idneys and led that an : parathion i. Details s drawn to Ping in the substances. i . Jones ru s msec,,. of Agr., 2), 143-5 ss tolerant itoxicating 1 Brown with lead i Vauxhall !), 316-19 -vtes (ob , in 0.85% acked cell 0-5 y Ph arkers (vs. increased ed group- 964 13773 69-- Toxicology and A ir Pollution 13774 Co: / J 7 7 ^ -cnificant increase of fragility was seen in 6 anemic patients. cumulation of effects despite intervals as long as 96 hrs. between The ty p e of coagulant used has no effect on fragility, but the exposure. Cutaneous exposures (head not exposed) for 2-, 4-, taiiied values are sensitive to the time of rotation during test and 6-hr. periods to 580, 550 and 710 p.p.m., resp., caused no ? g. 24 references. Andrew L. Reeves or min. signs of toxicity. Conens. of B in serums and urine were 'f iv e cases of anuria from (acute) carbon tetrachloride poison made but changes in the conditioned avoidance response proved . F. Heully, A. Larcan, G. Rauber, C. Huriet, G. Vaillant, a to be the most useful test in detecting early and residual effects ud M. C. Aug (Clin. Med. A, Nancy, France). Ann. Med. in dogs. Frank A. Smith Vnricy 2(Sept.), 1184-95(1963). Toxicological., pathol., and Experimental study on nitroglycerol poisoning in rabbits. hiochem. aspects are described. The effects (described) of CCL Effect of nitroglycerol on the blood. Hiromichi Hasegawa and " the kidneys were particularly marked^ with the production of Mitsuo Sato (Natl. Inst. Health, Kawasaki, Japan). J. Bio- general renal insufficiency. One of the 5 cases was fatal. _chem . (Tokyo) 54, 58-64(1963). Subcutaneous injection of W. C. Tobie nitroglycerol to rabbit (0.3 g./kg.) caused rapid increases in Toxicity of water enriched with silver ions. D. I. Lazarenko, methemoglobin content in blood and in the O affinity of the c v. Chizhov, G. I. Kozyrevskaya, N. A. Gaidamkin, and N. D. blood, in several hrs. These changes were restored approx, to makovskii. Gigiena i Sanit. 29(2), 98-100(1964). Daily the original levels in 24 hrs. No NOs-methemoglobin was de doses 4 mg- Ag+/kg. in the drinking water of rats increased the tectable in the blood after poisoning. Blood catalase activity 0 of leukocvtes, but did not otherwise produce any observable b was lowered sharply after nitroglycerol injection and it was re Effects on carbohydrate metabolism, blood compn. or histology. covered only partly in 24 hrs. F. K. Anan The amt. of Ag+ which would be used in H ,0 purification would Structural change of pyrophyllite by grinding, and its effect on o0t be objectionable. John Howe Scott toxicity of the cell. H. Hayashi, K. Koshi, A. Hamada, and H. Activation of the fibrinolytic system of the guinea pig following Sakabe (Natl. Inst. Ind. Health, Tokyo). Clay Set. (Tokyo) 1, inoculation of Echis colorata venom. B. M__o_av,_ _C_h_. _M_o_roz, 99-108(1962). Continued grinding of pyrophyllite (4-67 hrs.) md A. de Vries (Univ. Tel-Aviv, Israel). Tox^con 1(3), 109-12 results in progressive attenuation of the characteristic x-ray dif (1963) . The intravascular fibrinolysis occurring following infraction features of pyrophyllite and the formation of an ag jection of E. colorata venom in the guinea pig is due mainly to gregated amorphous product. Infrared absorption records show activation of its fibrinolytic system. Milton Feldstein loss of O-H (stretching) and H-O-Al (bending) frequencies, loss of Comparative toxicity of refrigerants. F. Caujolle (C.N.R.S., resoln. in Si-0 stretching features, and important absorption of Toulouse, France). Bull. Inst. Intern. Froul 44(1), 20-55 water. Dosages of the (amorphous) ground products to achieve a (1964) (in French and English). A review. SFTT standard toxic effect on monocyte cultures are 2-5 times those The significance of urine uranium excretion data. Morton necessary with unground pyrophyllite. _ W. F. Bradley Lippman, Long D. Y. Ong, and William B. Harris (U.S. At. Ornithine carbamyl transferase activity in biood serum and Energy' Comm., New York, N.Y.). Am. Ind. Hyg. Assoc. J. liver of guinea pigs after CC1< intoxication. V. Neuman, V. 25(1). 43-54(1964). Routine urine samples cannot be used to Kulhanek, V. Maderova, and K. Sindelarova (Vet. Fac. Res. monitor individual exposures or to det. chronic exposure levels. -- Inst. Traumatol., Brno, Czech.). Acta Vet. Acad. Set. Hung. Samples after the termination of the exposure can give estimates 13, 239-44(1963)(in English). Administration of CCU to ofexposure levels, future excretion rates, and body burdens. Wm. MacL. Pierce guinea pigs resulted in a marked increase of serum ornithine carbamyl transferase (I) beginning at 6 hrs. and reaching a max. Effect of DL-ethionine on the liver of dog and rabbit. Mario of 70-fold the normal level 48 to 72 hrs. after the injection. At Alvizouri and Jaime Cortes (Med. School, Univ. Michoacana de the same time liver activity of I decreased. At 72 to 96 hrs. San Nicolas, Hidalgo, Mexico). Arch. Pathol. 77, 57-63(1964). d after administration the enzyme activities of both serum and Dogs and rabbits were fed DL-ethionine and severe hepatic dam- liver were tending to normal values. W. N. Anderson age occurred, with hemorrhagic tendencies. The pancreatic Toxicology of organotin compounds. A literature review.-' A. lesions, which predominate after ethionine poisoning in the rat, M. Ivanitskii. Farmakol. i Toksikol. 26(5), 629y32( 1963). 28 were not severe. M. L. C. Bemheim references. Juk'-.n F. Smith Experimental intoxication of dogs with sodium fluoroacetate-- The ultrastructural changes that occur during the transforma- Clinical, anatomical, and histopathological investigation. F. tion of lung macrophages to giant cells and fibroblasts in expen- Guarda and U. Dotta (Univ. Studi Turin, Italy). Ann. Fac. mental asbestosis. J. M. G. Davis (Univ. Cambridge, Engl.). Med. Vet. Torino 12, 241-70(1962). In the acute expt., Na Brit. J. Exptl. Pathol. 44, 568-75(1963). A few days after ex- fluoroacetate (0.2-4 mg./kg.) produced excitement, myoclonus, posure of rats and guinea pigs to chrysotile asbestos dust the convulsions, and death within 1-3 hrs. in dogs. There weredif- lung macrophages carrying the dust fuse together by means of fuse hemorrhage in various parenchymas, cerebral edema, and e elongated processes and become giant cells. Fibroblasts were lymphocyte infiltration into the Virchow-Robin spaces. In found to contain chrysotile dust, suggesting the transformation chronic expts. (0.02 mg./kg. on alternate days) the intoxication of macrophages into fibroblasts. M. L. C. Bernheim caused degeneration of the parenchymas, lymphocytic encepha- Variability of the degree of provoked alcoholemia in the guinea litis and proliferation of the glial elements. GGJL pig. J. Seydoux and M. Fasel (Univ. Geneva, Switz.). -ririv. Biological action of beryllium. Reaction of the monkey to Physiol. Pharmacol. Acta 21(3), C65-C67(1963)(in French), inhaled aerosols. G. W. H. Schepers (Inst. Forensic Med. Toxicol., Newark, Del.). Ind. Med. Surg. 33, 1-16(1964). Monkeys were exposed to aerosols of BeFj (I), BeSO (II), and BeHPCL (HI) for 7-30 days. The exposure conens. were 5.2 y Be/cu. ft. for I and 5.6 y Be for II and III. In a second study monkeys (4/dose level) were exposed to conens. of HI of 5.6, 32, and 236 y Be/cu. ft. for 30, 10, and 8 days, resp. I showed the highest toxicity. One monkey exposed to III (5.6 y Be/cu. ft.) for a 30-day period died 45 days after termination of exposure. Exposures of monkeys to III at 32 and 236 y Be/cu. ft. for 8-10 days resulted in death to all monkeys within 82 days after ex posure. Seven of the 8 monkeys showed chem. pneumonitis. One monkey exposed to III (32 y Be/cu. ft. for 10 days) showed alveolar carcinoma 82 days after the exposure. Changes in the liver, kidney, adrenals, thyroid, and spleen were also observed in monkeys exposed to I and H. W. L. Downs Short-exposure inhalation toxicity of pentaborane in animals. Francis W. Weir, Van M. Seabaugh, Millard M. Mershon, David Guinea pigs were given 2.37 g./kg. of EtOH orally (enough to induce symptoms of inebriation) and blood samples were taken at intervals of 15 or 30 min. for the next 90 min. Blood ale. content at any particular time showed wide individual variations, ranging from 0.08 to 0.2% for the different animals. Sex or wt. of the individual was not a factor. L. E. Gilson Ethionine pancreatitis (in rats). O. Hartl, T. Muellner, A. Neumayr, and H. Pietschmann (Med. Universitaetsklin., Vienna). Acta Hepato-Splenol. 10(6), 368-78(1963). Groups of 10 female rats (150-200 g. wt.) were given 50, 100, 200, and 300 mg./lOO g. of DL-ethionine (I) in physiol, saline by stomach tube. The rats were held for 48 hrs. without food (but with water available), then were sacrificed by bleeding. The lowest dosage of I had no gross effects on the internal organs but the 200 and 300 mg./lOO g. doses produced extensive signs of acute pan creatitis and steatosis of the liver. The serum levels of various enzymes were detd. for each dose of I administered, in comparison 0 with the same enzymes in the serum of rats which had received G. Burke, and Maurice H. Weeks (Edgewood Arsenal, Md.). CCL (0.2 ml./lOO g.). Data are tabulated for serum alk. phos- Toxicol. Appl. Pharmacol. 6(1), 121--31(1964). The 5-, 10-, 30-, phatase (II), leucine aminopeptidase (III), glutamic-oxalacetic and 60-min. lethal concn.-50% values for rats exposed to BsHi>(I) transaminase (IV), lactate dehydrogenase (V), fructosediphos- Were 66.6, 31.2, 15.2 and 10.4 p.p.m., resp.; corresponding phoric acid aldolase (VI), malate dehydrogenase (VII), and values for mice were 40.5, 18.6, 10.6, and 7.8 p.p.m. Toxic_sorbitol dehydrogenase (VIII).Increasing amts, of I did not signs were tremors, ataxia, convulsions, a reddish exudate around have any consistent effects on the levels of II, III, and VI. As the mouth and nose, and death. Exposure of dogs for 5-, 15-, the doses of I increased, serum IV decreased moderately and Via and 60-min. periods to 26, 12, and 3 p.p.m. of I produced border- decreased sharply, while V and VII increased about 3- and 2-fold, line signs of toxicity. Daily repeated exposures at approx, these resp., from the lowest to the highest I dose. The rats which levels caused convulsions, apprehensiveness, scleral injection, received CC1< showed relatively high levels of all serum enzymes and miosis after the 2nd exposure. Single exposures at 9.3, a (in comparison with the rats which received the smallest amt. ot 5.0, and 1.4 p.p.m. for 5-, 15- and 30-min. periods, resp., pro- I) with the highest levels for V and VIII. Possible mechanisms ot duced no detectable effects, but daily exposure for 5 days caused action of I in producing pathol. organ changes and alterations m irritability, miosis, and increased response time in a conditioned serum enzymes are considered in relation to previous reports, avoidance-response test. Repeated exposure to 2.5 p.p.m. for 1 33 references. . W. t-.1 ooie hr. with intervals of 24-96 hrs. between exposures showed ac- The chronic oral toxicity of monomenc ethyl acrylate ana