Acute heat stress induces oxidative stress and decreases adaptation in young white leghorn cockerels by downregulation of avian uncoupling protein
Acute heat stress induces oxidative stress and decreases adaptation in young white leghorn cockerels by downregulation of avian uncoupling protein
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DOI：
10.1093/ps/86.2.364
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发表时间：
2007-02-01
期刊：
影响因子：
4.4
通讯作者：
Toyomizu, M.
中科院分区：
文献类型：
--
作者：
Mujahid, A.;Akiba, Y.;Toyomizu, M.
活性氧引起的细胞和分子损伤是热应激导致动物性能下降的机制之一。线粒体是细胞超氧化物的主要生产者，这是一个对质子动力敏感的过程，这种超氧化物的产生可以通过温和的解偶联来减少。研究了热应激对雏鸡和雏公鸡骨骼肌线粒体超氧化物产生的影响，以及热应激对鸡解偶联蛋白（avUCP）和鸡A核苷酸转运蛋白（avANT）表达的影响。雄性白色来航鸡（朱莉娅）在16日龄和公鸡在87日龄暴露于急性热应激，34摄氏度18小时，或保持在中等环境温度（25和21摄氏度，分别）。热暴露和对照鸡之间的线粒体超氧化物的产生没有差异，而在年轻的公鸡的情况下观察到显着差异。更大的底物非依赖性超氧化物的生产被发现在肌肉线粒体从热应激的年轻公鸡。在雏鸡中，无论是avUCP还是avANT的转录表达被热暴露改变，而在年轻的公鸡avUCP转录降低，但avANT的转录水平没有改变。因此，在热应激的年轻公鸡，增加线粒体超氧化物的产生伴随着下调avUCP。两者合计，这些结果表明，暴露的年轻公鸡热应激刺激线粒体超氧化物的产生，可能通过下调avUCP。另一方面，具有持续avUCP表达的雏鸡相对更好地适应高温。因此，推测avUCP的适当表达可以缓解线粒体超氧化物的过度产生，有助于鸟类对急性热应激引起的氧化应激的适应。
Reactive oxygen species-induced damage of cells and molecules is one of the mechanisms responsible for the decline in an animal's performance due to heat stress. Mitochondria are the main producers of cellular superoxide, a process that is sensitive to proton motive force, and this superoxide production can be decreased by mild uncoupling. We studied the effects of heat stress on the production of mitochondrial superoxide as well as heat stress effects on the expression of avian uncoupling protein (avUCP) and avian A nucleotide translocator (avANT) in skeletal muscles of chicks and young cockerels. Male White Leghorn (Julia) chicks at 16 d and cockerels at 87 d of age were exposed to acute heat stress, 34 degrees C for 18 h, or kept at moderate ambient temperature (25 and 21 degrees C, respectively). There was no difference in mitochondrial superoxide production between heat-exposed and control chicks, whereas significant differences were observed in the case of young cockerels. Greater substrate-independent superoxide production was found in muscle mitochondria from heat-stressed young cockerels. In chicks, neither avUCP nor avANT transcript expression was changed by heat exposure, whereas in young cockerels avUCP transcript was decreased, but avANT transcript level was not changed. Thus, in heat-stressed young cockerels, increased mitochondrial superoxide production was accompanied by downregulation of avUCP. Taken together, these results suggest that exposure of young cockerels to heat stress stimulates mitochondrial superoxide production, possibly via downregulation of avUCP. Chicks with persistent avUCP expression, on the other hand, are relatively better adapted to high temperature. It can be assumed that appropriate expression of avUCP may alleviate overproduction of mitochondrial superoxide and could help birds adapt to oxidative stress resulting from acute heat stress.