carbon disulfide/necrosis

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Protective action of diethyldithiocarbamate and carbon disulfide against renal injury induced by chloroform in mice.

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Oral administration of diethyldithiocarbamate (DTC) and carbon disulfide (CS2) protected mice against CHCl3-induced kidney injury, as evidenced by normalization of delayed plasma phenolsulfonphthalein clearance, suppression of increased kidney calcium content and prevention of renal tubular

Carbon disulfide exposure attenuates adrenergic inotropic response in rats.

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Catecholamine-induced myocardial necrosis is enhanced in carbon disulfide exposed rats. We investigated whether the reported morphological findings after carbon disulfide exposure are accompanied by functional disturbances of the adrenergic inotropic response as well as by biochemical alterations.

Changes in hepatic glutathione concentrations during carbon disulfide induced hepatotoxicity in the rat.

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When administered acutely to male Sprague-Dawley rats, carbon disulfide (CS2, 5 mmole/kg ip) caused centrilobular hepatic hydropic degeneration or necrosis. Pretreatment with phenobarbital was a requirement for hepatotoxicity and treatment with SKF 525-A, an inhibitor of microsomal CS2 metabolism,

Protective action of diethyldithiocarbamate and carbon disulfide against acute toxicities induced by 1,1-dichloroethylene in mice.

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In male mice of ddY strain, a single dose of 1,1-dichloroethylene (1,1-DCE, 0.1 ml/kg, ip) produced severe renal damage at 24 hr, as evidenced by elevations in plasma urea nitrogen concentration and kidney calcium content and by massive renal tubular necrosis, while hepatic damage was less severe. A

Carbon disulfide hepatoxicity and inhibition of liver microsome calcium pump.

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This work has shown that CS2 promptly inhibits the liver ER calcium pump only in those animals that subsequently develop hepatic necrosis. In this respect, inhibition of the ER calcium pump by CS2 resembles the actions of chlorinated hydrocarbon hepatotoxins. This lends further support to the

Styrene-induced hepatotoxicity in mice depleted of glutathione.

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In mice depleted of glutathione (GSH) by pretreatment with an inhibitor of GSH synthesis, buthionine sulfoximine (BSO; 1 hr before styrene, 2 mmol/kg or higher doses, ip), styrene (0.96-5.76 mmol/kg, po) produced hepatotoxicity characterized by an increase in serum alanine transaminase activity and

Hepatotoxicity of eugenol in mice depleted of glutathione by treatment with DL-buthionine sulfoximine.

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Eugenol is widely used as a food flavoring agent and a dental analgesic. Mice treated with eugenol (400-600 mg/kg, po) in combination with an inhibitor of glutathione (GSH) synthesis, buthionine sulfoximine (BSO; 1 hr before eugenol, 4 mmol/kg, ip) developed hepatotoxicity characterized by increases

Effects of drug metabolism modifiers on pulegone-induced hepatotoxicity in mice.

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Intraperitoneal injection of R-(+)-pulegone (pulegone), the main constituent of pennyroyal oil, to ddY mice caused extensive liver injury as characterized by an increase in serum glutamic pyruvic transaminase (GPT) activity and centrilobular necrosis of hepatocytes. Treatments of mice with the

Hepatotoxicity of butylated hydroxytoluene and its analogs in mice depleted of hepatic glutathione.

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Butylated hydroxytoluene (2,6-di-tert-butyl-4-methylphenol, BHT) has been reported to be a lung toxicant. Mice treated with BHT (200-800 mg/kg, po) in combination with an inhibitor of glutathione (GSH) synthesis, buthionine sulfoximine (BOS; 1 hr before and 2 hr after BHT, 4 mmol/kg per dose, ip)

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