Oxidative stress in cold-induced hyperthyroid state

Abstract

SUMMARYExposure 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 3,5,3Ј-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.

Activity of antioxidant enzymes in the liver of wild boars (Sus scrofa) from aselenium-deficient area depending on sex, age, and season of the year

“…On the one hand, it increases the production of ATP and of the heat necessary for maintaining normothermia; on the other hand, it is responsible for increasing the generation of ROS. Around 2%-5% of O 2 consumed by mammalian mitochondria does not undergo the complete 4-electron reduction to water and, as a result of electron leakage from the respiratory chain, it forms ·O 2 - (Venditti et al, 2010). In a dismutation reaction catalyzed by superoxide dismutase, this free oxygen radical is reduced to H 2 O 2 , which, in turn, is a substrate for Se-GSH-Px (there is no CAT in mitochondria), which transforms it into water and molecular oxygen (Lykkesfeldt and Svendsen, 2007;Limón-Pacheco and Gonsebatt, 2009).…”

Effects of powdery mildew infection on chloroplast and mitochondrial functions in rubber tree

“…The integrity of mitochondrial membranes was reduced by nearly 80% at 10 dai compared to the uninfected control leaves. Since mitochondria are an important location of the conversion of AOS to H 2 O 2 by SOD, their breakdown inevitably increases AOS content (Venditti et al, 2010). Oxidative damage in lipids, proteins, and DNA has been suggested as indexes of oxidative stress in biological systems.…”

Effects of dietary guanidinoacetic acid and betaine supplementation on performance, blood biochemical parameters and antioxidant status of broilers subjected to cold stress

“…Low ambient temperatures also cause increased feed intake (FI) and decreased nutrient digestibility, which in turn negatively influences the broiler performance. Also, cold stress causes oxidative stress in tissues such as heart, kidney, small intestine, thymus, adrenal glands and lungs (Venditti et al 2010). Cold temperature and rapid growth enhance the metabolic rate, which is followed by creating a high oxygen requirement, and causes an imbalance between the respiration system and the high oxygen requirement, leading to systemic hypoxia (Wideman & Kirby 1995), which increases production of reactive oxygen species (ROS) in mitochondria (Lu et al 2010).…”