Cold-induced hyperthyroidism produces oxidative damage in rat tissues and increases susceptibility to oxidants.

In this work, we investigated whether cold exposure-induced hyperthyroidism increases oxidative damage and susceptibility to oxidants of rat liver, heart and skeletal muscle. All tissues exhibited gradual increases in hydroperoxide and protein-bound carbonyl levels. Glutathione peroxidase activity increased in all tissues after 2 days and further increased in the muscle after 10 days of cold exposure. Liver glutathione reductase activity increased after 10 days of cold exposure, while heart and muscle activities were not modified. Vitamin E levels were not affected by cold, while coenzyme Q9 and coenzyme Q10 levels decreased in heart and muscle after 2-day cold exposure and were not further modified after 10 days. Liver coenzyme Q9 levels increased after 2 days whereas coenzyme Q10 levels increased after 10 days in the cold. The whole antioxidant capacity was lowered, while parameters positively correlated with susceptibility to oxidants were increased by cold. Lipid fatty acid composition was modified in all tissues. In particular, fatty acid unsaturation degree increased in heart and muscle. Cytochrome oxidase activity increased, suggesting an increased content of hemoproteins, which are able to generate .OH radical. This view was supported by the observation that the tissue susceptibility to H(2)O(2) treatment, which is strongly correlated to iron-ligand content, increased after cold exposure. In this frame, it is apparent that the increase in oxidative capacity, necessary for homeotherm survival in low temperature environments, has potential harmful effects, because it results in increased susceptibility to oxidative challenge.