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首页> 外文期刊>The journals of gerontology.Series A. Biological sciences and medical sciences >Free radical production, antioxidant capacity, and oxidative stress response signatures in fibroblasts from Lewis dwarf rats: effects of life span-extending peripubertal GH treatment.
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Free radical production, antioxidant capacity, and oxidative stress response signatures in fibroblasts from Lewis dwarf rats: effects of life span-extending peripubertal GH treatment.

机译：Lewis矮大鼠成纤维细胞中的自由基产生，抗氧化能力和氧化应激反应特征：延长寿命的青春期围生期GH治疗的影响。

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The discovery that in invertebrates, disruption of the insulin/insulin-like growth factor (IGF)-1 pathway extends life span and increases resistance to oxidative injury led to the hypothesis that IGF-1 signaling may play a role in regulating cellular reactive oxygen species production, oxidative stress resistance, and consequentially, organismal life span in mammals. However, previous studies testing this hypothesis in rodent models of IGF-1 deficiency yielded controversial results. The Lewis dwarf rat is a useful model of human growth hormone (GH)/IGF-1 deficiency as it mimics many of the pathophysiological alterations present in human GH/IGF-1-deficient patients as well as elderly individuals. Peripubertal treatment of Lewis dwarf rats with GH results in a significant extension of life span. The present study was designed to test the role of the GH/IGF-1 axis in regulating cellular oxidative stress and oxidative stress resistance, utilizing primary fibroblasts derived from control rats, Lewis dwarf rats and GH-replete dwarf rats. Measurements of cellular dihydroethidium and C-H(2)DCFDA fluorescence showed that cellular O(2)(.-) and peroxide production were similar in each group. Fibroblasts from control and Lewis dwarf rats exhibited similar antioxidant capacities and comparable sensitivity to H(2)O(2), rotenone, high glucose, tunicamycin, thapsigargin, paraquat, and mitomycin, which cause apoptosis through increasing oxidative stress, mitochondrial damage, ATP depletion, and/or by damaging DNA, lipids and proteins. Fibroblasts from GH-replete rats exhibited significantly increased antioxidant capacities and superior resistance to H(2)O(2), rotenone and bacterial lipopolysaccharide-induced cell death compared with cells from Lewis dwarf rats, whereas their sensitivity to the other stressors investigated was not statistically different. Thus, low circulating IGF-1 levels present in vivo in Lewis dwarf rats do not elicit long-lasting alterations in cellular reactive oxygen species generation and oxidative stress resistance, whereas life span-extending peripubertal GH treatment resulted in increased antioxidant capacity and increased resistance to cellular injury caused by some, but not all, oxidative stressors.
机译：在无脊椎动物中，胰岛素/胰岛素样生长因子（IGF）-1途径的破坏延长了寿命并增加了对氧化损伤的抵抗力的发现导致了以下假设：IGF-1信号传导可能在调节细胞活性氧中起作用生产，抗氧化应激性以及相应地哺乳动物的生物寿命。但是，先前在IGF-1缺乏症的啮齿动物模型中测试该假设的研究产生了有争议的结果。刘易斯矮人大鼠是人类生长激素（GH）/ IGF-1缺乏症的有用模型，因为它模仿了人类GH / IGF-1缺乏症患者以及老年人的许多病理生理变化。 GH对Lewis矮人大鼠的青春期耻骨周围治疗可显着延长寿命。本研究旨在测试GH / IGF-1轴在调控细胞氧化应激和氧化应激抗性中的作用，该实验利用了来自对照大鼠，刘易斯矮人大鼠和GH矮人大鼠的原代成纤维细胞。细胞二氢乙啶和C-H（2）DCFDA荧光的测量结果表明，每组细胞中的O（2）（.-）和过氧化物的产生均相似。来自对照和刘易斯矮人大鼠的成纤维细胞显示出相似的抗氧化能力和对H（2）O（2），鱼藤酮，高葡萄糖，衣霉素，thapsigargin，百草枯和丝裂霉素的敏感性，它们可通过增加氧化应激，线粒体损伤，ATP引起细胞凋亡。消耗和/或破坏DNA，脂质和蛋白质。与来自Lewis矮大鼠的细胞相比，来自生长激素充足的大鼠的成纤维细胞显示出显着提高的抗氧化能力和对H（2）O（2），鱼藤酮和细菌性脂多糖诱导的细胞死亡的优异抗性，而对其他应激源的敏感性却没有统计上不同。因此，在刘易斯矮鼠体内存在的低循环IGF-1水平不会引起细胞活性氧种类的产生和氧化应激抗性的长期改变，而延长寿命的青春期围生期GH处理导致抗氧化能力增强和抗氧化能力增强细胞氧化损伤是由某些（但不是全部）氧化应激因素引起的。

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