Abstract
The administration of cobaltous chloride to rats produced a selective dose-dependent decrease in the cytochrome P-450 component of the microsomal electron transport system. A concommitant of the alteration in microsomal electron transport components was a refractoriness to the carbon tetrachloride-induced elevation in serum glutamic oxaloacetic transaminase (SGOT), serum glutamic pyruvic transaminase (SGPT), isocitric dehydrogenase (ICDH), and the decrease in hepatic microsomal glucose-6-phosphatase activity. Cobaltous chloride pretreatment also decreased the intensity of microsomal diene conjugation absorption observed after carbon tetrachloride administration. The results support the concept that cytochrome P-450 is the site of production of toxic metabolites following carbon tetrachloride intoxication.
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