Document Nw6qQEgY5yDM1gEa8Jv0b22g

* T------ v*.w w, ^ spnndiitg spots, eluting t!ic II with EtO*' indfktg. colorimetri- gaily. The extn. yield was ~-80%.. nonary tests showed 5''* no II in eiin. healthy personnel, while among the staff of I-prnc- ' cosing plants, HU'/, of the sampled persons gave 3 pos. reaction _ to the method. Extensive tests showed that most of the pos. reactions were obtained with stun" employed 11-5 years in the plants. In the*.'; eases the prcciiiograms were modified, the o- globulin fraction being ^higher and the y-glnbuhn fraction being If er than ill the persons with neg. reactions to the pres* rpee of II in the urine. It was concluded that the capacity of' the organism to metabolise II decreased after 2 years. M. Ben Elicscr 1240g Effect of hexachloro-p-xylene ingestion on the oxidative phosphorylation of rat liver mitochondria. Hsia-Ying Chang and Chcn-To Yuan (Sino-Sovict Friendship IIosp., Peking, China). Sheng ll'w Hua Hsueh Yu Sheng IFu Wit Lt Hsuek Pao 6(3), 273-5(19G6)(Ch). Oral administration of hexachloro-p- xylcnc (I, 0.5 g./kg./day) to rats uncoupled the oxidative phos phorylation of the liver mitochondria, in extent proportional to the duration of I treatment. The decrease in the production of ATP with insufficient energy supply of tissue may be the basis of the toxic reactions of I such as generalized weakness, fatigue, dizziness, headache. BHJJ 1241q Adrenaline-inactivation capacity of the normal and of the CCLi-poisoned liver perfused in vitro. Emma Costiner, L. Vaislcr, and Viorica Chivu (Acad. Rep. Soc., Romania, Bu charest). Sludii Circetarx Endocrinol. 17(4), 355-7( 19fl6)(R.om). Normal rat livers, and livers originating from CCl,-trcatcd rats were perfused with adrenaline in vitro. The latter showed a lower rate of adrenaline degradation as compared with the former. BTJQ 1242X Pyruvic avid content in acute barbiturate poisoning. B. F. Murashov (S. M. Kirov Mil. Med. Acad., Leningrad). Ttr. Arkh. 38(10), 103--l(1906)(Russ). In deep coma due to barbiturate intoxication, 1.2 mg. % pyruvic acid (I) was found in the blood. Its concn. decreased with recovery to 0.77 mg. %. When the I concn. reached 1,8-2 mg. %, complications occurred and the respiration was disturbed. The I concn. was directly proportional to the severity of intoxication, as observed in a total of 32 poisoned humans. Miloslav Kalab 1243e Inhibition of biosynthesis of protein and nucleic acids by phenolic compounds in vivo, G. V. Kukushkina, L. B. Gor,- bacheva, and N. M. Emanuel (lust. Chcm. Phys., Moscow). ^ Vopr. Mtd. Khim. 12(5), 452-5( 196G)(Russ). Mice with the Ehrlich ascites carcinoma or solid hepatoma XXII were injected with a mixt. of uniformly "C-lubcled L-amino acids (I) (10 ^c./ mouse), Na formate "C (II) (o /uc.) or adenine--uC (III) (17 pc.). After 30 min., one group was injected intraperitoneally with Pr gallate (IV) in 0.9% NaCl and another, with 4-methyl- 2,6-di-lerf-butylphcnol (V) in 3% aq. Tween-80. Controls were injected with the resp. solvents. Ascitic fluid samples were taken from mice with Ehrlich tumors at time intervals from 0 to 180 min. and the cells washed with a 5:4 1 mixt. of 0.9% NaCl, 0.3Af NaiHPO,, and 0.3,1/ KHiPOt. Mice with solid tumors were sacrificed after 120 min. and the tumors, liver, kidneys, and spleen were removed and homogenized. When I was used, the cells were treated with cold 5% CljCCOOH and the pptd. pro teins isolated and exaind. When II and III were used, 5% Clj CCOOH washings were extd. with Et,0, the aq. layer evapd., and the residue (acid-sol. fraction) examd. for radioactivity. The acid-insol. fraction was washed with cold 9G% EtOH and heated for 10 min. at 50 with EtOH-EtjO (2:1) to remove lipids. A sample was examd. for radioactivity and the rest extd. with 10% NaCl (pH 7.4-7.6) for 30 mm. at 95. Nucleic acids were pptd. by adding 3 vols. of cold 9G% EtOH and washed with 70% EtOH. In mice with ascites tumors, injection of 75 mg./ kg. of V decreased 1 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 tug. of V/kg. inhibited III incor|xiration almost completely. Injec tion of 80 mg. of IV/kg. or of 120 mg. of V/kg. alter 150 min. de creased II incortxiration into acid-inxol. fraction by 43-55%, into nucleic acid by 54-01% , into acid-sol. fraction by 50-77%, and into proteins, by 30 44%. In mice with solid hepatoma, in jection of 150 mg. of IV/kg. after 150 nun, decreased I incorpora tion into tumor proteins by 20%; 200 mg. of IV/kg. decreased I incorporation by 03%. Injection of 150-200 mg./kg, of IV had no effect on protein biosynthesis in kidne ys and the liver of normal mice and in kidneys of tumor.hearing mice- eelhch sin,wed some activation of I inenrpor.ilion pi the liver. Injection of 200 - *ng. of IV/kg. decreased I incorporation into spleen proteins of normal and tumor-bearing mice by 30%,; 150 mg./kg, had no effect on prntc-iu biosynthesis in the spleen. Fells Bonk 1244n Experiment?! intoxication by ammonium salts. Pro tection by some amino acids and their mechanism of action. F. k imiiio and K. Salvatore I Univ. Naples). HioiIiiiii. ,!/>/>/. 13 2', o7 H5( ldlili)(I|.,I), The Inoe lu m. ennver-i,,n ,,f Nil, into urea is dise'iissed relative In the protection ,iHorded in acute and chronic Mill intoxication hy some com|sK, assoed. with the con version process. Exptl acute NHi poisoning was produced in rats by administering D. NHjOAc, preceded by varying doses of protective at..... ... acids and their mixts. Based on mortality and convulsions, arginine (I) provides the most effec tive protection at as tow a dose as 0.5 millimole/kg. A mixt. (A) of Gomithinc and L-aspartic acid at a dose of 1.0 millimole/ kg. protects as effectively as 1. A comparison of bf-'od NH and urea levels using I and A shows I to be more effective a pro tector than A. In rats intoxicated with a L.D.uof NHtOAc and protected by A, o-methylaspartic acid injected intraperitoneally in a dose of 3.4 tnillimoles/kg. produces approx. 54% mortality and 90% convulsions. Utilizing this same procedure but sub stituting I for .1, the mortality and convulsions percentages de crease. Further, a dose of 0.5 millimole I/kg. produces 8.8% mortality and 20% convulsions, while a dose of 1.0 millimole I 'kg. produces 21 % mortality and 38% convu'sions, 67 refer ences. Domcnic A. Yavala 1245v Erythrocytic ALA dehydratase and lead. D. Bonsig* nore, P. Cahssano, and C. CartasejAia (Univ. Genoa). Pan- minerva Med. (Engl. Ed.) 6(7-8), 282-4(I966)(Eng). Persons having Pb poisoning showed an increased urinary excretion of aminolevulinic acid (ALA) (I), which was assoed. with a sig nificantly decreased activity of I dehydratase in the erythrocytes. The assay of I dehydratase may be of significance in assessing the gravity of Pb poisoning, since in exptl. animals the level of I dehydratase was related to the extent of the poisoning. B. S. S. R- Rao 1246c Relations between the porphyrin metabolism and the nicotinic acid metabolism in saturnine poisoning. L. Pecora, A. Silvestroni. and A. Brancaccio (Univ. Naples). Panminerva }Ied. (Engl. Ed.) 8(7-8), 284-8(1966)(Eng). Poisoning of rab bits with Pb(0Ac)j decreased nicotinic acid (I) by 75% in the blood and urine and markedly increased erythiocyte-frce proto porphyrin (II) (13-247 y %) and urinary coproporphyrin (III) (14--341 7/24 hrs.), aminolevulinic acid (IV) (0.2-21 mg./l.), porphobilinogen (V) (trace-6.6 mg./l.), and xanthurenic acid (VI) (1.0-18.3 mg./24 hrs.). I administration either concurrently with or 15 days after Pb poisoning increased nicotincmia and nicotinuria and markedly inhibited (by 50-80%) the effects of Pb poisoning on II, III, IV, V, and VI. The effects of Pb poison ing are probably mediated through inhibition of pyridine coen- .-yme synthesis directly or indirectly through vitamin Bt inhibi tion. HFJN 12471c Porphyrins in tetraethyl lead poisoning. M. Crepet and P. Chiesura (Univ, Padua, Italy). Panminerva Med. (Engl. Ed.) 8(7-8), 295-301(1966)(Eng). The levels of aminolevulinic arid, Pb, and porphyrins were detd. in blood and urine samples oi persons having Pb poisoning due to inorg. Pb salts or Pb tetraethyl and also in exptl. animals with exptl. Pb poisoning. Pb poisoning due to Pb tetraethyl caused a significant increase in the levels of free protoporphyrin in erythrocytes, while Pb poi soning due to inorg. Pb salts caused an increased unnary excre tion of aminolevulinic acid and coproporphyrin. B. S. S. R. Rao 1248t Afiatoxin B, injury in rat and monkey liver. Donald J. Svoboda, Harold Grady, and John Higginson (Univ. of Kan sas, Med. Center, Kansas City). Amer. J. Pathol. 49(6), 1023- 51(19G6)(Eng). Oral administration of pure afiatoxin Bi (0.45- 3.78 mg./kg.) or intraperitoncal injection of a 0.167-mg./kg. dose into rats produced periportal parenchymal cell necrosis and slight bile duct proliferation, together with sepn. of the granular and fibrillar components of the nucleolus with the formation of nucleolar caps. The alterations in fine structure were also found in monkeys after oral administration of 0.45 mg. purified afia toxin B^kg. or intraperitoncal injection of a 2.5-mg./kg. dose. The livers of rats receiving an oral 0.45-tng./kg. dose 24-72 hrs. before sacrifice showed decreased levels of RNA and protein in both the nucleus and cytoplasm. The RNA-fo-DNA ratio in a total liver homogenate decreased by 40%, and that in a nuclear fraction by 8%; the protcin-to-DNA ratio in the total homoge nate decreased by 24%. P:0 ratios showed decreasing values with increasing functional damage to the hepatic mitochondria after administration of afiatoxin B|. Both O consumption and phosphorylation were inhibited, although the essentially normal O consumption 72 hrs. after administration of the toxin may have indicated recovery of respiration without the concomitant return to normal phosphorylation levels. The acute hepatic lesions shown by light microscopy of liver from treated monkeys re sembled the changes in human liver during acute viral hepatitis. Administration of pure afiatoxin Ui (1 ppm. of a synthetic diet fed ad libitum to rats fur 33 weeks) did not produce the nuclear, nucleolar, and cytoplasmic alterations found after the acute administration, although well-differentiated hepatuccllular carci nomas appeared in rats whose livers otherwise stiowed little ab normality. 55 references. B1*JN 1249a Distribution and excretion of cyclamate-uC sodium in animals. Jonathan 1*. Miller, I,. E. Michael Crawford, Robert C Sunders, and Earl Y. Cardinal (Dept, of I'harmaCol., Abbott I.ali'., North Chiengn). lUmhcm. liiiiphys, Hi'i. Cum Ml. 25(2), 153-7(l!NU>)(Eng). Na cyclainatc-uC' distribution, excretion. BOR 009706