Oxidative stress in marathon runners:: interest of antioxidant supplementation
Oxidative stress in marathon runners:: interest of antioxidant supplementation
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DOI：
10.1079/bjn20061696
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发表时间：
2006-08-01
影响因子：
3.6
通讯作者：
Vina, Jose
中科院分区：
文献类型：
--
作者：
Gomez-Cabrera, Mari-Carmen;Martinez, Agustin;Vina, Jose
我们最近报道，黄嘌呤氧化酶参与产生的自由基在力竭运动。别嘌呤醇，黄嘌呤氧化酶的抑制剂，防止it. The本工作的目的是阐明的作用，运动衍生的活性氧在细胞信号转导通路中参与的适应运动man. We发现，运动导致血浆黄嘌呤氧化酶的活性增加和NF-κ B B在外周血淋巴细胞活化后马拉松运行。这种激活是依赖于自由基的形成，在行使：治疗别嘌呤醇完全prevents it. In动物模型，我们以前表明，NF-κ B B激活引起的力竭性体育锻炼导致超氧化物歧化酶，参与抗氧化防御的酶的表达增加。我们报告的证据表明，活性氧在运动中作为信号，因为减少其形成可以防止激活重要的信号通路，这可能会导致有用的适应细胞。
We have recently reported that xanthine oxidase is involved in the generation of free radicals in exhaustive exercise. Allopurinol, an inhibitor of xanthine oxidase, prevents it. The aim of the present work was to elucidate the role of exercise-derived reactive oxygen species in the cell signalling pathways involved in the adaptation to exercise in man. We have found that exercise causes an increase in the activity of plasma xanthine oxidase and an activation of NF-kappa B in peripheral blood lymphocytes after marathon running. This activation is dependent on free radical formation in exercise: treatment with allopurinol completely prevents it. In animal models, we previously showed that NF-kappa B activation induced by exhaustive physical exercise leads to an increase in the expression of superoxide dismutase, an enzyme involved in antioxidant defence. We report evidence in man that reactive oxygen species act as signals in exercise as decreasing their formation prevents activation of important signalling pathways which can cause useful adaptations in cells.