%0 Journal Article
%T Up-regulation of avian uncoupling protein in cold-acclimated and hyperthyroid ducklings prevents reactive oxygen species production by skeletal muscle mitochondria
%A Benjamin Rey
%A Damien Roussel
%A Caroline Romestaing
%A Maud Belouze
%A Jean-Louis Rouanet
%A Dominique Desplanches
%A Brigitte Sibille
%A St¨¦phane Servais
%A Claude Duchamp
%J BMC Physiology
%D 2010
%I BioMed Central
%R 10.1186/1472-6793-10-5
%X The abundance of avUCP mRNA, as detected by RT-PCR in gastrocnemius muscle but not in the liver, was markedly increased by cold acclimation (CA) or pharmacological hyperthyroidism but was down-regulated by hypothyroidism. Activators of UCPs, such as superoxide with low doses of fatty acids, stimulated a GDP-sensitive proton conductance across the inner membrane of muscle mitochondria from CA or hyperthyroid ducklings. The stimulation was much weaker in controls and not observed in hypothyroid ducklings or in any liver mitochondrial preparations. The production of endogenous mitochondrial reactive oxygen species (ROS) was much lower in muscle mitochondria from CA and hyperthyroid ducklings than in the control or hypothyroid groups. The addition of GDP markedly increased the mitochondrial ROS production of CA or hyperthyroid birds up to, or above, the level of control or hypothyroid ducklings. Differences in ROS production among groups could not be attributed to changes in antioxidant enzyme activities (superoxide dismutase or glutathione peroxidase).This work provides the first functional in vitro evidence that avian UCP regulates mitochondrial ROS production in situations of enhanced metabolic activity.The respiratory chain function of mitochondria constitutes a major cellular source of superoxide and derived reactive oxygen species (ROS) in vivo [1,2]. ROS, including hydroxyl and hydroperoxyl radicals, can alter mitochondrial and cellular lipid membranes, proteins and nucleic acids and may be implicated in various pathological diseases, accelerated senescence and aging [2,3]. Different protective and adaptive responses can prevent an imbalance between oxidant production and antioxidant capacities, eventually repair oxidative damage and thereby limit the deleterious effects of ROS [2,4]. These responses include several powerful antioxidant enzymes such as superoxide dismutase (SOD), catalase and glutathione peroxidase. Nevertheless, other mechanisms for reducing ROS
%U http://www.biomedcentral.com/1472-6793/10/5