thiobarbituric-acid and Carbon-Tetrachloride-Poisoning

A comparative study of the hepatoprotective effect of carnosine and 4-methyluracil under CCl4-induced acute toxic hepatitis has been carried out. The extent of liver injury and its regeneration were established from morphological data as well as from changes in the activities of alanine aminotransferase (ALT) and histidase and the bilirubin content in blood serum. Hyperlipoperoxidation in the liver and serum was assessed by the amount of TBA-active products. It was found that by day 10 of experimental hepatitis ALT and histidase levels in blood sera of untreated animals exceeded the normal values 1.3- and 3.9-fold, whereas those in the carnosine-treated group approximated the values characteristic of intact animals. The activity of serum ALT in animals treated with vitamin B12 or 4-methyluracil exceeded normal values 1.5 and 1.6 times, whereas that of histidase was 2.5 and 2.7 times as high. Carnosine and 4-methyluracil inhibited (in approximately the same degree) the formation of TBA-active products in the liver. According to morphological dta, cessation of CCl4 injections was accompanied by rapid regeneration of liver tissues in all animal groups. Carnosine enhanced regenerative processes in parenchymatous and connective tissues in a far greater degree in comparison with other drugs. The mitotic index in the carnosine-treated group exceeded more than twofold the corresponding parameters in untreated animals. Possible mechanisms of carnosine action on liver repair are discussed.

Topics: Alanine Transaminase; Animals; Carbon Tetrachloride Poisoning; Carnosine; Chemical and Drug Induced Liver Injury; Histidine Ammonia-Lyase; Lipid Peroxidation; Liver; Male; Rats; Thiobarbiturates; Uracil; Vitamin B 12

The profiles of lipid peroxidation products in liver homogenates or microsomal membranes prepared from CCl4-intoxicated mice were determined by several commonly employed methods. The level of conjugated dienes peaked within 30 min and then decreased, suggesting the transitory nature of lipid peroxides in vivo. Values for thiobarbituric acid positive material peaked 30 min after CCl4 treatment, diminished thereafter for a time, and gradually rose to a new maximum at 24 h; the first peak appears to represent lipid peroxides and the second represents further degradation products including malondialdehyde. Fluorescence intensity (excitation, 360 nm; emission, 430 nm) was closely correlated with the second peak. Our findings support the involvement of lipid peroxidation in CCl4-induced hepatotoxicity in mice and emphasize the necessity for several analytical indices of lipid peroxidation performed at different time intervals.

Topics: Animals; Carbon Tetrachloride Poisoning; Female; Lipid Peroxides; Liver; Mice; Microsomes, Liver; Thiobarbiturates

Topics: Animals; Carbon Tetrachloride Poisoning; Hydrogen-Ion Concentration; Liver; Male; Rats; Rats, Inbred Strains; Sodium Dodecyl Sulfate; Thiobarbiturates

Topics: Animals; Carbon Tetrachloride Poisoning; In Vitro Techniques; Lipid Peroxides; Liver; Male; Malondialdehyde; Rats; Rats, Inbred Strains; Thiobarbiturates

It has been suggested that lipid peroxidation is an important factor in the pathogenesis of carbon tetrachloride (CCl4) hepatotoxicity. In the present work, experimental liver injury induced by CCl4 was inhibited by the immunopotentiators such as BCG, levamisole, PS-K, and OK-432, and despite exposure to CCl4 the liver tissue levels of thiobarbituric acid (TBA) reactive substances were not increased in rats pretreated with immunopotentiators. Though immunopotentiators exhibit a protective action against CCl4-induced lipid peroxidation damage, their clinical role and mechanism of protective action on the liver have yet to be clarified in detail.

Topics: Adjuvants, Immunologic; Alanine Transaminase; Animals; Aspartate Aminotransferases; BCG Vaccine; Biological Products; Carbon Tetrachloride Poisoning; Chemical and Drug Induced Liver Injury; Female; Levamisole; Liver; Picibanil; Proteoglycans; Rats; Rats, Inbred Strains; Thiobarbiturates; Vitamin E

Experimental liver disorders were induced by the use of carbon tetrachloride or D-galactosamine hydrochloride in rats maintained on a vitamin E deficient diet and in rats fed a diet supplemented with vitamin E, and the protective effect of vitamin E on the liver was determined. After exposure to carbon tetrachloride or D-galactosamine hydrochloride the serum levels of transaminases, lysosomal enzyme beta-glucuronidase, and acid phosphatase were elevated, and thiobarbituric acid reactive substances in serum and liver homogenate were also increased. The changes were conspicuous in the vitamin E deficient rats, but were only slight in rats fed a diet supplemented with vitamin E. The results of this study suggest that vitamin E has a protective effect on liver disorders by inhibiting lysosomal enzyme liberation and lipid peroxidation.

Topics: Animals; Carbon Tetrachloride Poisoning; Chemical and Drug Induced Liver Injury; Female; Galactosamine; Liver; Lysosomes; Rats; Rats, Inbred Strains; Thiobarbiturates; Vitamin E

Topics: Animals; Carbon Tetrachloride Poisoning; Chlorobenzenes; Hexachlorobenzene; Lipid Peroxides; Male; Organ Size; Rats; Rats, Inbred Strains; Thiobarbiturates; Tissue Distribution

Topics: Animals; Carbon Tetrachloride Poisoning; Lipid Peroxides; Liver; Male; Rats; Rats, Inbred Strains; Thiobarbiturates