Oxidative stress in cold-induced hyperthyroid state.

Exposure of homeothermic animals to low environmental temperature is associated with oxidative stress in several body tissues. Because cold exposure induces a condition of functional hyperthyroidism, the observation that tissue oxidative stress also happens in experimental hyperthyroidism, induced by 3,5,3'-triiodothyronine (T(3)) treatment, suggests that this hormone is responsible for the oxidative damage found in tissues from cold-exposed animals. Examination of T(3)-responsive tissues, such as brown adipose tissue (BAT) and liver, shows that changes in factors favoring oxidative modifications are similar in experimental and functional hyperthyroidism. However, differences are also apparent, likely due to the action of physiological regulators, such as noradrenaline and thyroxine, whose levels are different in cold-exposed and T(3)-treated animals. To date, there is evidence that biochemical changes underlying the thermogenic response to cold as well as those leading to oxidative stress require a synergism between T(3)- and noradrenaline-generated signals. Conversely, available results suggest that thyroxine (T(4)) supplies a direct contribution to cold-induced BAT oxidative damage, but contributes to the liver response only as a T(3) precursor.