Tetrabutyrate on Inactivation of Rat Liver Microsomal Enzymes Induced by Carbon Tetrachloride 1

It has been postulated that hepatotoxicity of carbon tetrachloride is related to its prooxidant effect on lipid peroxidation (1-8). DIANZANI and UGAZIO (8) reported that several antioxidants, i.e., propyl gallate, N, N•L-diphenyl-p-phenyl enediamine, and reduced glutathione, which are administered to rats prior to carbon tetrachloride, inhibit significantly the accumulation of hepatic triglycerides. Preventive effect on hepatic injury is also observed for ƒ¿-tocopherol (9-10). It has also been reported that some microsomal enzymes are inactivated by dosing rats with carbon tetrachloride and that inactivation is prevented by administration of antioxidants prior to hepatotoxin (11-14). Furthermore, it was observed that inactivation of membrane-bound enzymes is associated with production of malon aldehyde (7, 15, 16), which is known to be formed from the decomposition of