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锌缺乏的氧化应激。

The oxidative stress of zinc deficiency.

机构信息

Department of Nutritional Sciences, University of Wisconsin-Madison, 1415 Linden Drive, Room 340B, Madison, WI 53706-1571, USA.

出版信息

Metallomics. 2011 Nov;3(11):1124-9. doi: 10.1039/c1mt00064k. Epub 2011 Jul 26.

DOI:10.1039/c1mt00064k
PMID:21789324
Abstract

Zinc is an essential catalytic and structural cofactor for many enzymes and other proteins. While Zn2+ is not redox active under physiological conditions, it has been known for many years that zinc deficiency causes increased oxidative stress and, consequently, increased oxidative damage to DNA, proteins, and lipids. These results have indicated that zinc plays an indirect antioxidant role and that dietary inadequacy may contribute to human diseases such as cancer. Recent studies are helping to identify the primary sources of oxidative stress in low zinc. In addition, through studies of the model eukaryotic cell, Saccharomyces cerevisiae, we are now beginning to understand the strategies cells use to limit this stress and reduce its damage.

摘要

锌是许多酶和其他蛋白质的必需催化和结构辅助因子。虽然在生理条件下,Zn2+ 没有氧化还原活性,但多年来人们已经知道,缺锌会导致氧化应激增加,从而导致 DNA、蛋白质和脂质的氧化损伤增加。这些结果表明,锌发挥间接抗氧化作用,饮食不足可能导致人类疾病,如癌症。最近的研究有助于确定缺锌引起的氧化应激的主要来源。此外,通过对模式真核细胞酿酒酵母的研究,我们现在开始了解细胞用来限制这种应激并减少其损伤的策略。

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