CHANGES IN THE LEVELS OF ENDOGENOUS COENZYME-Q HOMOLOGS, ALPHA-TOCOPHEROL, AND GLUTATHIONE IN RAT-LIVER AFTER HEPATIC ISCHEMIA AND REPERFUSION, AND THE EFFECT OF PRETREATMENT WITH COENZYME-Q10

  • 1 January 1984
    • journal article
    • research article
    • Vol. 797  (1) , 1-9
Abstract
Whether hepatic ischemia and the subsequent reflow of blood had any effect on the levels of endogenous coenzyme Q homologs, .alpha.-tocopherol and glutathione, and whether coenzyme Q10 (6 mg/kg of body wt) altered these levels was determined. Ischemia of the rat iver for 90 min resulted in decreases of 19.1 and 19.6% of endogenous .alpha.-tocopherol and total glutathione (GSH [reduced glutathione] + GSSG [oxidized glutathione]) without significant changes in the levels of endogenous total coenzyme Q homologs (oxidized and reduced). Restoration of the blood flow resulted in marked decreases in endogenous coenzyme Q homologs, .alpha.-tocopherol and total glutathione in the control group. In coenzyme Q10-treated animals, however, there were no changes in the levels of endogenous total coenzyme Q9, .alpha.-tocopherol or total glutathione as well as in the level of the enhanced total coenzyme Q10 during the reperfusion period. On the other hand, decreases in .alpha.-tocopherol and total glutathione during the period of ischemia remained unchanged. These results are compatible with the assumption that cellular damage caused by hepatic ischemia can be explained by free radical reaction processes during ischemia and especially, reperfusion and suggest that exogenous coenzyme Q10 functions as an antioxidant with endogenous coenzyme Q homologs, .alpha.-tocopherol and glutathione in lipid peroxidation during reperfusion.

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