Sequential changes in superoxide production, anion carriers and substrate oxidation in skeletal muscle mitochondria of heat-stressed chickens
Sequential changes in superoxide production, anion carriers and substrate oxidation in skeletal muscle mitochondria of heat-stressed chickens
复制标题
DOI：
10.1016/j.febslet.2007.06.051
复制
发表时间：
2007-07-24
期刊：
影响因子：
3.5
通讯作者：
Toyomizu, Masaaki
中科院分区：
文献类型：
--
作者：
Mujahid, Ahmad;Akiba, Yukio;Toyomizu, Masaaki
我们已经证明，热应激鸟类在骨骼肌线粒体中表现出增加的超氧化物生产。为了确定这种影响的确切机制，我们不仅研究了热应激鸡线粒体中超氧化物产生、阴离子载体和底物氧化的渐进变化，还研究了其顺序变化。暴露于急性热应激（34℃持续6、12和18小时）刺激胸肌线粒体超氧化物的产生。热应激诱导的avUCP基因转录本下调和线粒体avUCP蛋白含量下调具有时间依赖性：热应激6 h后avUCP基因转录本降低，而热应激12 h后avUCP蛋白含量下调。禽类腺嘌呤核苷酸转位子（avANT）基因转录本在热应激下未发生改变，表明avANT可能不参与热应激鸡肌肉线粒体超氧化物产生的调节。在急性热应激初期，β -氧化酶基因转录本和活性上调，血浆非酯化脂肪酸水平升高，线粒体脂肪酸运输基因表达增加。线粒体底物氧化的突然激增导致超氧化物的产生增加：热应激后6小时的avUCP表达可能不足以缓解活性氧（ROS）的过量产生，尽管线粒体中可能存在少量内源性FFA（一种潜在的解耦剂）。此后，avUCP含量下调，而底物氧化恢复到控制水平。avUCP的下调可能导致线粒体超氧化物产生增加，在热应激后期保持高超氧化物产生。这些结果表明，在热应激条件下，鸡骨骼肌线粒体ROS的过量产生可能是由于底物氧化增强和avUCP的下调以一种时间依赖性的方式引起的。(c) 2007年欧洲生化学会联合会。Elsevier B.V.版权所有。
We have shown that heat-stressed birds exhibit increased superoxide production in skeletal muscle mitochondria. To determine the precise mechanism for this effect, here we studied not only progressive, but also sequential changes in superoxide production, anion carriers and substrate oxidation in mitochondria of heat-stressed chickens. Exposure to acute heat stress (34 degrees C for 6, 12 and 18 h) stimulated pectoralis muscle mitochondrial superoxide production. Heat stress-induced downregulations of avUCP gene transcripts and mitochondrial avUCP protein content were time-dependent: avUCP gene transcript was decreased after 6 h, while avUCP protein content was only downregulated after 12 h of heat stress. Avian adenine nucleotide translocator (avANT) gene transcripts were not changed on exposure to heat stress, suggesting that avANT may not be involved in the regulation of superoxide production in the muscle mitochondria of heat-stressed chickens. During the initial stage of acute heat stress beta-oxidation enzymes gene transcripts and activity were upregulated, with elevated plasma non-esteritied fatty acid levels and increased expression of mitochondrial fatty acid transport genes. This sudden surge in mitochondrial substrate oxidation resulted in higher superoxide production: the avUCP expression at 6 h after heat stress might have not been large enough to alleviate the overproduction of reactive oxygen species (ROS) even though a small amount of endogenous FFA, a potential uncoupler, might have been present in the mitochondria. Thereafter, avUCP content was downregulated while substrate oxidation returned to control levels. This downregulation of avUCP may have caused increased mitochondrial superoxide production, keeping the superoxide production high in the later stages of heat stress. These results suggest that overproduction of mitochondrial ROS in chicken skeletal muscle under the heat stress might result from enhanced substrate oxidation and downregulation of avUCP in a time-dependent manner. (c) 2007 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.