ubiquinone and Carbon-Tetrachloride-Poisoning

Antioxidants in the blood plasma of rats were measured as part of a comprehensive, multilaboratory validation study searching for noninvasive biomarkers of oxidative stress. For this initial study an animal model of CCl(4) poisoning was studied. The time (2, 7, and 16 h) and dose (120 and 1200 mg/kg, intraperitoneally)-dependent effects of CCl(4) on plasma levels of alpha-tocopherol, coenzyme Q (CoQ), ascorbic acid, glutathione (GSH and GSSG), uric acid, and total antioxidant capacity were investigated to determine whether the oxidative effects of CCl(4) would result in losses of antioxidants from plasma. Concentrations of alpha-tocopherol and CoQ were decreased in CCl(4)-treated rats. Because of concomitant decreases in cholesterol and triglycerides, it was impossible to dissociate oxidation of alpha-tocopherol and the loss of CoQ from generalized lipid changes, due to liver damage. Ascorbic acid levels were higher with treatment at the earliest time point; the ratio of GSH to GSSG generally declined, and uric acid remained unchanged. Total antioxidant capacity showed no significant change except for 16 h after the high dose, when it was increased. These results suggest that plasma changes caused by liver malfunction and rupture of liver cells together with a decrease in plasma lipids do not permit an unambiguous interpretation of the results and impede detection of any potential changes in the antioxidant status of the plasma.

Topics: Animals; Antioxidants; Ascorbic Acid; Biomarkers; Carbon Tetrachloride Poisoning; Disease Models, Animal; Electron Spin Resonance Spectroscopy; Free Radicals; Glutathione; Liver; Oxidative Stress; Rats; Rats, Inbred F344; Ubiquinone; Uric Acid; Vitamin E

It has been suggested that lipid peroxidation is an important factor in the pathogenesis of carbon tetrachloride (CCl4) hepatotoxicity. In the present study, experimental liver injury induced by CCl4 could be inhibited by Coenzyme Q10 (CoQ10) and in spite of exposure to CCl4 the liver tissue levels of thiobarbituric acid (TBA) reacting substances were not increased in rats pretreated with CoQ10. In the in vitro experiment as well, the apparent liver tissue levels of TBA were decreased after addition of CoQ10. These facts provided evidences that CoQ10 possessed a direct antioxidative effect and protected against CCl4 hepatotoxicity by this antioxidative effect.

Topics: Animals; Antioxidants; Carbon Tetrachloride; Carbon Tetrachloride Poisoning; Chemical and Drug Induced Liver Injury; Female; Liver; Rabbits; Thiobarbiturates; Ubiquinone

Topics: Animals; Carbon Tetrachloride Poisoning; Chemistry Techniques, Analytical; Chromatography, Paper; Diabetes Mellitus, Experimental; In Vitro Techniques; Liver; Mitochondria; Rats; Subcellular Fractions; Succinate Dehydrogenase; Ubiquinone

Topics: Carbon Tetrachloride Poisoning; Electron Transport Complex II; Fatty Liver; Mitochondria; Seasons; Succinate Dehydrogenase; Ubiquinone