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首页> 外文期刊>The Journal of Experimental Biology >Physiological adaptations to reproduction. I. Experimentally increasing litter size enhances aspects of antioxidant defence but does not cause oxidative damage in mice
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Physiological adaptations to reproduction. I. Experimentally increasing litter size enhances aspects of antioxidant defence but does not cause oxidative damage in mice

机译:对繁殖的生理适应。 I.实验性增加垫料大小可增强抗氧化能力,但不会引起小鼠氧化损伤

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摘要

Life history theory suggests that investment in reproduction can trade off against growth, longevity and both reproduction and performance later in life. One possible reason for this trade-off is that reproduction directly causes somatic damage. Oxidative stress, an overproduction of reactive oxygen species in relation to cellular defences, can correlate with reproductive investment and has been implicated as a pathway leading to senescence. This has led to the suggestion that this aspect of physiology could be an important mechanism underlying the trade-off between reproduction and lifespan. We manipulated female reproductive investment to test whether oxidative stress increases with reproduction in mice. Each female's pups were cross-fostered to produce litters of either two or eight, representing low and high levels of reproductive investment for wild mice. No differences were observed between reproductive groups at peak lactation for several markers of oxidative stress in the heart and gastrocnemius muscle. Surprisingly, oxidative damage to proteins was lower in the livers of females with a litter size of eight than in females with two pups or non-reproductive control females. While protein oxidation decreased, activity levels of the antioxidant enzyme superoxide dismutase increased in the liver, suggesting this may be one pathway used to protect against oxidative stress. Our results highlight the need for caution when interpreting correlative relationships and suggest that oxidative stress does not increase with enhanced reproductive effort during lactation.
机译:生命史理论表明,对生殖的投资可以与生命的增长,寿命以及生命后期的生殖和性能进行权衡。这种折衷的可能原因之一是生殖直接造成了身体的损害。氧化应激是一种与细胞防御有关的活性氧过剩的产生,可能与生殖投资有关,并被认为是导致衰老的途径。这导致人们提出生理学的这一方面可能是在生殖和寿命之间进行折衷的重要机制。我们操纵雌性生殖投资来测试氧化应激是否随着小鼠生殖而增加。每只雌性的幼犬被交叉育种以产生二胎或八胎的产仔,这代表了野生小鼠生殖投资的高低水平。在心脏和腓肠肌的几种氧化应激标志物,在泌乳高峰期的生殖组之间没有发现差异。出人意料的是,窝产仔数为8的雌性动物的肝脏对蛋白质的氧化损伤低于有两只幼崽或非生殖对照的雌性动物。尽管蛋白质氧化减少,但肝脏中抗氧化酶超氧化物歧化酶的活性水平增加,这表明这可能是用于抵御氧化应激的一种途径。我们的结果强调了在解释相关关系时需要谨慎的态度,并表明氧化应激不会随着泌乳期间生殖能力的增强而增加。

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