Antioxidant-sensitive triiodothyronine effects on characteristics of rat liver mitochondrial population.

Whole mitochondrial population and three mitochondrial fractions were resolved by differential centrifugation from liver homogenates from euthyroid, hyperthyroid (ten daily i.p. injections of triiodothyronine (T3), 10 microg/100 g body weight) and hyperthyroid vitamin E-treated (ten daily i.m. vitamin E injections, 20 mg/100 g body weight) rats. Homogenates and mitochondrial preparations were examined for their protein content, oxidative capacity, lipid peroxidation, antioxidant status, and susceptibility to oxidative stress. In all groups, antioxidant level was smaller and oxidative capacity, lipid peroxidation, and susceptibility to oxidants were greater in the heavy mitochondrial fraction. T3 treatment was associated with increased oxidative capacity, lipid peroxidation, and susceptibility to oxidative stress, and decreased antioxidant levels in all preparations. It was also associated with increased mitochondrial protein content of homogenate and altered quantitative presence of the mitochondrial fractions. The vitamin E effects on the T3-induced changes were different for the different parameters. Vitamin E did not modify the mitochondrial protein content in liver and oxidative capacity of the various preparations, reduced the changes in both susceptibility to oxidants and contribution of each fraction to the whole mitochondrial population, and reinstated euthyroid values for antioxidant capacity and lipid peroxidation. The incomplete recovery of euthyroid resistance to oxidants in vitamin E-treated rats is due to the vitamin inability to reinstate the levels of both antioxidants and hemoproteins, on which such a resistance depends. The vitamin E effect on the composition of the mitochondrial population is more difficult to explain, because of the complexity of the mechanisms underlying the mitochondrial population modulation by thyroid hormone. However, available data suggest that such a modulation occurs through changes in the turnover of the mitochondrial fractions to which an induction of mitochondrial protein synthesis and accelerated antioxidant-sensitive degradation contribute in different measure.