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Hepatic Phosphoglucomutase Activity as a Marker of Oxidative Stress Induced by Pro-oxidative Drugs.

A decrease in hepatic phosphoglucomutase activity was found after intraperitoneal doses to rats with pro-oxidative drugs; carbon tetrachloride, ethanol, paraquat, phenobarbital, thiopental, 3-methylcholanthrene, benzo[a]pyrene, Trp-P-1, benzene, and polychlorinated biphenyl. When the drugs were given at half of their LD50 values, except ethanol, hepatic phosphoglucomutase activities were decreased, and aldehydes which were detected by the thiobarbituric acid test were simultaneously accumulated 24 h after administration, in the liver. A significant correlation between phosphoglucomutase activity and the accumulations of aldehydes was obtained (r = - 0.536). No other changes in hepatic enzymes and metabolites were commonly observed. On the other hand, the low-molecular-weight aldehyde fraction in secondary products of linoleic acid decreased phosphoglucomutase activity in hepatocytes cultured with dexamethasone. It was concluded that aldehydes originating from endogenous lipid peroxidation decreased phosphoglucomutase activity in the liver, and the assay of hepatic phosphoglucomutase activity was useful as a marker of oxidative stress induced by pro-oxidative drugs.