Effects of dithiocarb the (+)-cyanidanol-3 on the hepatotoxicity and metabolism of vinylidene chloride in rats
Abstract
The acute hepatotoxic effects of vinylidene chloride (VDC) were evidenced by measurement of the increase in the serum of the aminotransferase (GPT) and sorbitol dehydrogenase (SDH), hepatic glutathione (GSH) depletion and histological examinations in rats. The hepatoprotective agents dithiocarb and (+)-cyanidanol-3 proved well able to antagonize these toxic effects of VDC. While dithiocarb inhibited the in vivo metabolism of VDC in a closed exposure system, (+)-cyanidanol-3 had no influence at all. These findings substantiate the role of the microsomal monooxygenase system in the metabolism and hepatotoxicity of VDC. The mechanisms by which dithiocarb and (+)-cyanidanol-3 act as antihepatotoxic agents are different: the inhibition of the metabolic activation by dithiocarb and free radical-scavenging by (+)-cyanidanol-3.
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Cephaloridine-induced lipid peroxidation initiated by reactive oxygen species as a possible mechanism of cephaloridine nephrotoxicity
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Effects of diethyldithiocarbamate and nickel chloride on glutathione and trace metal concentrations in rat liver
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Protective action of diethyldithiocarbamate and carbon disulfide against acute toxicities induced by 1,1-dichloroethylene in mice
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Mechanistic aspects of enhanced lipid peroxidation following glutathione depletion in vivo
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