维生素E可以防止运动引起的DNA损伤

Andreas Hartmann , Andreas M. Nieβ , Martina Grünert-Fuchs , Bertram Poch , Günter Speit
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引用次数: 179

摘要

采用单细胞凝胶试验(SCG试验或彗星试验)研究了人单次剧烈运动后外周血细胞(WBC) DNA损伤及补充维生素的效果。人类受试者被要求在跑步机上跑步直到精疲力竭,并在跑步前和跑步后24小时采集血样。在所有先证者的24小时样本中观察到DNA链断裂明显增加。短期应用复合维生素片或维生素E (3 × 800 mg)可导致某些先证者白细胞中DNA效应的显著较小的增加。当志愿者在跑步前14天补充维生素E(每天1200毫克)时,所有先证者的运动引起的DNA损伤明显减少。在五分之四的研究对象中,补充维生素完全防止了剧烈运动后引起的DNA损伤。摄入维生素E 14天导致血清维生素E浓度明显升高。丙二醛(MDA),脂质过氧化的标志物,测定先证者的血清在试验中添加和不添加维生素14天。补充维生素E后,MDA浓度显著降低,但在跑步后15分钟和24小时变化不显著。我们的研究结果表明,维生素E可以防止运动引起的DNA损伤,并表明在穷尽性运动后氧化应激导致的白细胞DNA断裂。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Vitamin E prevents exercise-induced DNA damage

The single cell gel test (SCG test or comet assay) was used to study DNA damage in peripheral white blood cells (WBC) of humans after a single bout of exhaustive exercise and the effect of vitamin supplementation. Human subjects were asked to run on a treadmill until exhaustion and blood samples were taken before and 24 h after the run. A clear increase in DNA strand breakage was observed in the 24-h sample of all probands. A short-term application of multivitamin pills or vitamin E (3 × 800 mg) resulted in a significantly smaller increase of DNA effects in WBC of some probands. When the volunteers were given a supplement of vitamin E (1200 mg daily) for 14 days prior to run, exercise-induced DNA damage was clearly reduced in all probands. In four out of five subjects, vitamin supplementation completely prevented the induction of DNA damage after exhaustive exercise. Intake of vitamin E for 14 days led to a clear increase in vitamin E serum concentrations. Malondialdehyde (MDA), a marker of lipid peroxidation, was measured in the serum of probands in tests with and without vitamin supplementation for 14 days. MDA concentrations were significantly decreased following vitamin E supplementation but not significantly changed 15 min and 24 h after a run. Our results demonstrate that vitamin E prevents exercise-induced DNA damage and indicate that DNa breakage occurs in WBC after exhaustive exercise as a consequence of oxidative stress.

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