Document zdN7DGL8NwweYVp33pze6jE4m

*0591 Chemical Abstracts Vol. 69, 1966 N 47JJ I wicfc, N.J.). Can. J. Pkyriol. Pharmacol. 1968, 46(4), 609-16 (Eat). A series o( expts. has shown that the mechanisms by - which the metabolism of EtOH oe-;irs are strongly influenced by the partial pressures of the O present m the aerating medium. Por the most i equenlly user, gas mixt., 95% Oi 4- 5% CO, the EtOH consumption as abnormally large, and proportional to the concn. of EtOH in the perfusate. However, when the system was aerated with 18% 0 + 5% CO + 77% Ni, the consumption of EtOH was similar to that found in the intact rat. The perfusate concn. of MciCO, HOAc, pyruvic acid, and lactic acid was measured in alt expts. When EtOH was con sumed at these two different rates, increases in the lactic:* pyruvic ratio and acetate levels of the perfusate were noted in both types of expts. However, the utilization of glucose by isolated perfused liver was inhibited, and acetone levels in creased markedly, when EtOH was consumed at abnormally rapid rates, although no effect was noted in the perfusate levels of these metabolites when EtOH was consumed at normal rates. 27 references. RCYD 50591p Action of beryllium ions on primary cultures of swine cells. Vegni Talluri, Maria; Guiggani, Viviana (Univ. Siena, Siena, Italy). Caryologia 1967, 20(4), 355-67 (Eng). The effect of Be** poisoning on mitosis and morphology of swine kidney cell and lymphocyte cultures was studied. Treatment with Be** had a harmful effect on all the mitotic phases and abnormality of chromosomes was frequent. At high concns. the action of Be++ was less pronounced on kidney cells than on lymphocytes. Be++ exerts its toxic action by competition with Mg'1"* either ;n the activation of DNA polymerase or in the binding of DM.-, to histones. L. Mirone 50592q Protecti re effect of ethyl alcohol towards cllyl alco hol-induced hepatic lesions. Schwarzmann, V.; In/ante, R.; Raisonnier, A.; Caroli, J. (CHU Saint-Antoine, Paris, Fr,). C. R. Soc. Bull. 1967, 161(12), 2425-9 (Fr). A 90-min. per fusion of isolated rat liver with blood contg. allyl ale. (0.018 ml./ 180 ml.) caused a release of lactic dehydrogenase, malic dehy drogenase, and glutamic-pyruvic transaminase into the perfusate and a simultaneous depletion of these enzymes from the liver; ale. dehydrogenase and glutamic dehydrogenase activities were not detected in the perfusate and were not decreased in the liver. Biliary secretion was irreversibly arrested after 18-20 min. of perfusion, and hepatic lesions occurred. A 20-min. per fusion with blood contg. EtOH prior to the treatment with allyl ale. prevented the enzyme release, the hepatic lesi ns and the effect on biliary secretion, and did not cause the release of ale. dehydrogenase or glutamic dehydrogenase activities. BPJF 50593r Effect of ethanol on hepatic metabolism and enzyme activities. Nelson, Patricia Ann (Indiana Univ,, Blooming ton, Indiana). 1967, 104 pp. (Eng). Avail. Univ. Microfilms, Ann Arbor, Mich., Order No. 68-7228. From Diss. Abstr. B 1968,28(111,4688. SNDC 50594a Energy-linked calcium transport in liver mitochondria during carbon tetrachloride intoxication. Cars.foh, Ernesto; Tiozzo, Roberta (Umv. Modena, Modena. Italy). Exp. Mol. Pathol. 1968, 9(1), 131-40 (Eng). In rats intoxicated by the gas tric intubation of 0.5 ml. CCU/200 g,, Ca*'1' concn. m liver mito chondria increased --10-fold within 18-20 hrs. However, i.p. injected "Ca was not taken up by hepatic mitochondria in in toxicated rats as rapidly as in normal animals. In vitro, hepatic mitochondria from CCl-mtoxicated rats did not show increased C**+ uptake, but Ca1* release induced by oxidative phosphoryla tion uncouplers was greatly decreased. This suggested that in CCU intoxication, the balance between ADP phosphorylation nd Ca'* uptake is shifted in favor of the latter, thus contribut ing to the accumulation of Ca** in mitochondria. DDJN S0595t Protective effects of alpha-tocopherol on the hepato- toxicity of carbon tetrachloride: an electron microscope study. Meldoiesi, Jacopo (Inst. Pharmacol., Umv. Milan, Milan. Italy). Exp. Mol. Pathol. 1968, 9(1), 141-7 (Eng), The oral administra tion of 2.5 ml./kg. CCUdild. 1:2 with liq. paraffin to rats produced severe hepatic lesions within 24 hrs. However, liver damage was markedly reduced m rats i.p. injected with the lipid antioxidant, a-tocopherol succinate (125 mg./kg.), before CCU administra tion. This suggested that lipid peroxidn. is the primary mecha nism of CCU hepatotoxicity, 27 references. DDJN 50596u Distribution and toxicity of aliphatic hydrocarbons in body tissues. Shugacv, B, B. (Yaroslav, hied. Inst., Yaroslavl, USSR)- Farmahol. Toksibol. 1908, 31(3). 360-3 (Russ), Gas chromatog. was used to study the distribution of 6 volatile hy drocarbons m the mouse and rat body tissues. The volatile hydrocarbon content of the brain and parenchymatous organs was similar, but the level in the fatty tissue was significantly higher than in the brain, liver, kidneys, or spleen. There was a parallel between the toxicity and effective cerebral concn. of iso- prene, divinyl, and isobutylene, but not of butane, 2-mctliylpcnt- 1-ene, or 2-mcthylpcnt-2-cne. The divmyl concn, was higher in the medulla oblongata than in the cerebellum or cerebral cortex. BJJK 50597v Some biochemical changes in animals following acute polyethylene polyamine poisoning, boimmskaya, E. A, (Naucli.- Issted. Inst. Onkol., Leningrad, USSR). Farmahol. Tohsikol. 1968, 31(3), 364-5 (Russ). Polyethylene polyamine (750 mg,/ kg.) administered s.c. to rats and mice increased the hepatic monoamine oxidase and histammase activities, decreasing the tyramine and histamine levels in the blood and organ of the poisoned animals. The pathol. disturbances observed in mice and rats with acute polyethylene polyamine poisoning may be due to the increased oxidative deamination of endogenous amines with the consequent formation of aldehydes, NH, and HiO|. BJJR 5059SW Effect of niacin on phagocytosis In chronic trinitro toluene poisoning. Pidemskii, E. L.; Chukichev, E. M.; Mut'mcnko, A. M. (Perm. Univ., Perm, USSR). Farmahol. Tohsikol. 1968, 31(3), 365-6 (Russ). Trinit-otoluene (TNT) administered orally at 30 mg./kg. daily for 6 Jays to rats pro gressively decreased phagocytosis. Niacin administered simul taneously at 1 mg./kg. s.c. prevented this decrease and even in creased the phagocytic activity of the leukocytes to l.5-timcs the level in control rats, BJJR 50599x Pathogenic effect of chronic exposure to vinyl chloride on rabbits. Vazm. A. N.; Plokhova, E. 1. (Inst. Gig. Tr. Prof- zabol., Gorki, USSR). Farmahol. Tohsikol. 1968, 31(3), 369- 72 (Russ). In rabbits exposed to vinyl chloride (9-10 mg./I. air) for 4 hrs. daily for 5.5 months altered 0-waves (frequency >80 Hz.) appeared on the electroencephalogram from the an terior hypothalamic nuclei, and the potentials of the anterior and posterior nuclei increased by 18-30 and 70-85%, resp., over control values. Concomitant changes in the cardiovascular sys tem (bradycardia, arrhythmia, decreased voltage of the in dividual electrocardiogram peaks or whole complexes, decreased duration of systole, increased arterial pressi.re, and retarded blood flow) also occurred. The functional changes in the an terior and posterior hypothalamic nuelci may have a rote in the pathogenesis of toxic angioneurosis due to vinyl chloride. BJJR 50600r Brown FK. m. Administration of Ugh doses to rata and mice. Grasso, P.; Gaunt, 1. F.; Hall. D. E.; Golberg, L.; Batstone, Elizabeth (Brit. Ind. Biol. Res. Assoc., Carshal- ton, Engl.). Food Cosmet. Toxicol. 1968, 6(1), 1-11 (Eng). Acute oral toxicity studies with Brown FK gave LDm values >2 g./kg. and 8 g./kg. in mice and rats, resp. The values for i.p. injection were 1.5-2 g./kg. in mice and 0.75-1.15 g./kg. in rats. When repeated daily oral doses ranging from 0.1 to 2 g./kg. were given ta rats, a precipitous wt. loss and a vacuolar myopathy of the heart and skeletal muscles accompanied by lipofuscin formation occurred with doses of 0.5 g./kg. and over. At the highest dose employed (2 g./kg.), there was also hepatic centri- lobular necrosis and renal tubular degeneration Pretreatment with antibiotics reduced the incidence of muscle lesions. Re peated i.p. injection did not have any effect on the heart or skeletal muscle. Only 2 of the 6 components of Brown FK, 2,4-diamino- 5-(p-sulfophenyIazo)toluene (I) and 1,3-diamino-4-(p-sulfo- phenylazo)benzene (II), produced muscle damage after repeated oral doses of 0.5 g./kg. Comparable doses of mixts. contg. the other components as well as I or II were considerably less toxic. After daily oral doses of 1 g./kg., muscle lesions were found in rats, rabbits, and guinea-pigs, but none were seen in mice or hamsters. The results suggest that the intestinal micoflora is responsible for the breakdown of the components of Brown FK to toxic products. Variations between species and between ani mals of the same species may be due to qual. and quant, dif ferences in the intestinal microbial population. RCNP 50601s Brown FK. IV. Cytopathic effects of Brown FK on cardiac and skeletal muscle in the rat. Grasso, P.; Muir, A.; Golberg, L.; Batstone, Elizabeth (Brit. Ind. Biol. Res. Assoc., Carshalton, Engl.). Food Cosmet. ToxicoU 1968, 6(1), 13-24 (Eng). Administration of 2 or 3 massive (1 g./kg.) oral doses of Brown FK to rats induced a myopathy in cardiac and skeletal muscles characterized by multiple vacuoles --1-2 a in diam. Ultrastructurally, these consisted of areas of fibrillolysis, af fecting initially the A-band. Histochem., the myopathy was accompanied by a moderate increase in acid phosphatase activity and by a loss of phosphorylase activity. Subsequently, complete lysis of the affected fibers ensued. In the heart, lysis was fol lowed by macrophage invasion and fibroblastic proliferation, and in skeletal muscle, by regeneration. The occurrence of lipofuscin in muscle fibers and in macrophages was scanty and erratic. When Brown FK was given in the diet at a level of 21 i, fibrillolysis and an increase in the no. and electron d. of lyso- somes was observed ultrastructurally during week 2-3 of the test. These changes were accompanied by a marked elevation of histochem. demonstrable acid phosphatase. Progressive deposition of lipofuscin was the principal pathological feature during week 3-12. initial damage to the A- and [-bands in both cardiac and skeletal muscle distinguishes the Brown FK myop athy from that known to be produced by high doses of corti costeroids. tliyrxixiiie, cliloroqitntc. or plnsmociil. from ischemic damage and from muscle damage resulting from deprivation <>f K, Ca, or Mg. The lysosomal changes anil accumulation of lipofuscin arc suggestive of primary lysosomal damage which BOR 0 0 9 7 1 1