Functional argument for the existence of an avian nitric oxide synthase in muscle mitochondria: Effect of cold acclimation

Abstract

We report the first evidence of a mitochondrial NO synthase (mtNOS) in bird skeletal muscle. In vitro, mtNOS activity stimulated by L-arginine reduced intermyofibrillar mitochondrial oxygen uptake and ATP synthesis rates, stimulated endogenous H(2)O(2) generation, but had no effect on oxidative phosphorylation efficiency. Arginine-induced effects were fully reversed by L-NAME, a known NOS inhibitor. When ducklings were cold exposed for 4 weeks, muscle mitochondria displayed an increased state 3 respiration, a reduced H(2)O(2) generation but no significant alteration in mtNOS activity. We conclude that mtNOS is expressed in avian skeletal muscle.

The effect of selenium and polysaccharide of Atractylodes macrocephala Koidz. (PAMK) on endoplasmic reticulum stress and apoptosis in chicken spleen induced by heat stress

“…The overproduction of NO contributes to numerous pathological processes. 21 Several studies have demonstrated the importance of NOS-mediated signaling in many ES models. The research of Zhang et al demonstrated that both acute and chronic cold stress may cause duodenum oxidative stress and change in iNOS, which was related to the intestinal damage process.…”

Expression patterns and adaptive functional diversity of vertebrate myoglobins

“…In the heart, NO may also reversibly inhibit mitochondrial respiration by competing with O 2 for binding to cytochrome c oxidase in the respiratory chain, an effect that is more pronounced during hypoxia [91,92]. Inhibition of respiration by NO has also been demonstrated in the heart and skeletal muscle of numerous non-mammalian vertebrates, including fish, turtles and birds [93][94][95].…”

Thyroid status affects membranes susceptibility to free radicals and oxidative balance in skeletal muscle of Muscovy ducklings (Cairina moschata)

“…However, in contrast to the flourishing literature in mammalian models, very little data is available on how TH affects oxidative status in birds. As far as we know, it has been shown that, unlike rodents, cold‐ and pharmacologically induced hyperthyroidism reduces the rate ROS generated by muscle and liver mitochondria in Muscovy ducklings (Rey et al, , , ). This original mitochondrial flexibility observed in an hypermetabolic states has been interpreted as a compensatory mechanism that prevents an over generation of ROS in tissues, where mitochondrial content and oxidative fluxes are stimulated (Rey et al, ).…”