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首页> 外文期刊>Mechanisms of Ageing and Development >Manipulation of in vivo iron levels can alter resistance to oxidative stress without affecting ageing in the nematode C. elegans
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Manipulation of in vivo iron levels can alter resistance to oxidative stress without affecting ageing in the nematode C. elegans

机译：体内铁水平的控制可以改变对氧化应激的抵抗力，而不会影响线虫秀丽隐杆线虫的衰老

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Iron-catalyzed generation of free radicals leads to molecular damage . in vivo, and has been proposed to contribute to organismal ageing. Here we investigate the role of free iron in ageing in the nematode . Caenorhabditis elegans. Media supplementation with Fe(III) increased free iron levels . in vivo, as detected by continuous-wave electron paramagnetic resonance spectroscopy and elevated expression of the iron-sensitive reporter transgene . pftn-1::gfp. Increased free iron levels caused elevated levels of protein oxidation and hypersensitivity to . tert-butyl hydroperoxide (t-BOOH) given 9. mM Fe(III) or greater, but 15. mM Fe(III) or greater was required to reduce lifespan. Treatment with either an iron chelator (deferoxamine) or over-expression of . ftn-1, encoding the iron sequestering protein ferritin, increased resistance to . t-BOOH and, in the latter case, reduced protein oxidation, but did not increase lifespan. Expression of . ftn-1 is greatly increased in long-lived . daf-2 insulin/IGF-1 receptor mutants. In this context, deletion of . ftn-1 decreased . t-BOOH resistance, but enhanced both . daf-2 mutant longevity and constitutive dauer larva formation, suggesting an effect of ferritin on signaling. These results show that high levels of iron can increase molecular damage and reduce lifespan, but overall suggest that iron levels within the normal physiological range do not promote ageing in . C. elegans.
机译：铁催化的自由基的产生导致分子损伤。在体内，并已提出有助于机体衰老。在这里我们研究了游离铁在线虫衰老中的作用。秀丽隐杆线虫。添加Fe（III）的培养基会增加游离铁水平。体内，如通过连续波电子顺磁共振波谱和铁敏感的报告基因转基因表达升高所检测。 pftn-1 :: gfp。游离铁水平升高引起蛋白质氧化水平升高和对。过敏。给定叔丁基氢过氧化物（t-BOOH）为9. mM Fe（III）或更高，但需要15 mM Fe（III）或更高才能降低使用寿命。用铁螯合剂（去铁胺）或过表达的治疗。 ftn-1编码铁螯合蛋白铁蛋白，提高了对铁的抗性。 t-BOOH，在后一种情况下，减少了蛋白质的氧化，但没有增加寿命。的表达。长期使用ftn-1大大增加。 daf-2胰岛素/ IGF-1受体突变体。在这种情况下，删除。 ftn-1减少。 t-BOOH抗性，但两者均增强。 daf-2突变体的长寿和组成性dauer幼虫的形成，表明铁蛋白对信号传导有影响。这些结果表明，高水平的铁可增加分子损伤并降低寿命，但总体而言，正常生理范围内的铁水平不会促进衰老。秀丽隐杆线虫。

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