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Acute heat stress induces oxidative stress and decreases adaptation in young white leghorn cockerels by downregulation of avian uncoupling protein

机译:急性热应激通过禽解偶联蛋白的下调诱导年轻的白色来亨鸡的氧化应激并降低其适应性

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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.
机译:活性氧引起的细胞和分子损伤是热应激导致动物机能下降的机制之一。线粒体是细胞超氧化物的主要生产者,该过程对质子动力很敏感,轻度解偶联可降低这种超氧化物的产生。我们研究了热应激对线粒体超氧化物生产的影响,以及热应激对雏鸡和年轻公鸡骨骼肌中禽解偶联蛋白(avUCP)和禽A核苷酸转运蛋白(avANT)表达的影响。将16 d的雄性白来亨鸡(Julia)雏鸡和87 d的小公鸡暴露于34摄氏度的急性热胁迫下18 h,或保持在适当的环境温度下(分别为25和21摄氏度)。暴露于热的雏鸡和对照雏鸡之间的线粒体超氧化物产生没有差异,而在年轻的公鸡中观察到显着差异。在热应激的幼小公鸡的肌肉线粒体中发现了与底物无关的更大的超氧化物产生。在雏鸡中,暴露于热暴露既不改变avUCP转录也不表达avANT转录表达,而在年轻的公鸡中avUCP转录表达降低,但avANT转录表达水平未改变。因此,在热应激的年轻公鸡中,线粒体超氧化物的产生增加,同时伴随着avUCP的下调。综上所述,这些结果表明,可能通过下调avUCP,使年轻的公鸡暴露于热应激下会刺激线粒体超氧化物的产生。另一方面,具有持续avUCP表达的小鸡相对更适应高温。可以假定avUCP的适当表达可以减轻线粒体超氧化物的过量产生,并可以帮助禽类适应由急性热应激引起的氧化应激。

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