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线粒体:线粒体活性氧生成途径中的 omega-3。

Mitochondria: omega-3 in the route of mitochondrial reactive oxygen species.

机构信息

UMR 1198 Biologie du Développement et de la Reproduction, Institut National de la Recherche Agronomique, Département de Physiologie Animale, Jouy-en-Josas, France.

出版信息

Int J Biochem Cell Biol. 2012 Sep;44(9):1569-73. doi: 10.1016/j.biocel.2012.06.003. Epub 2012 Jun 15.

DOI:10.1016/j.biocel.2012.06.003
PMID:22710344
Abstract

Mitochondria are the main organelles that produce reactive oxygen species (ROS). Overproduction of ROS induces oxidative damage to macromolecules, including lipids, and can damage cellular membrane structure and functions. Mitochondria, the main target of ROS-induced damage, are equipped with a network of antioxidants that control ROS production. Dietary intake of omega-3 polyunsaturated fatty acids (ω3PUFAs) and consequently the increase in ω3PUFA content of membrane lipids may be disadvantageous to the health because ROS-induced oxidative peroxidation of ω3PUFAs within membrane phospholipids can lead to the formation of toxic products. Mitochondrial control of lipid peroxidation is one of the mechanisms that protect cell against oxidative damage. This review discusses the role of mitochondria in ROS generation and the mechanisms by which it regulates ROS production. The susceptibility to peroxidation of PUFAs by ROS raises the question of the adverse effects of ω3PUFA dietary supplementation on embryonic development and prenatal developmental outcomes.

摘要

线粒体是产生活性氧(ROS)的主要细胞器。ROS 的过度产生会导致包括脂质在内的大分子发生氧化损伤,并可能破坏细胞膜的结构和功能。作为 ROS 诱导损伤的主要靶点,线粒体配备了抗氧化剂网络来控制 ROS 的产生。ω-3 多不饱和脂肪酸(ω3PUFAs)的饮食摄入,以及随之而来的膜脂中 ω3PUFA 含量的增加,可能对健康不利,因为膜磷脂中 ROS 诱导的 ω3PUFA 氧化过氧化会导致有毒产物的形成。线粒体对脂质过氧化的控制是保护细胞免受氧化损伤的机制之一。本文讨论了线粒体在 ROS 产生中的作用以及它调节 ROS 产生的机制。PUFAs 被 ROS 过氧化的易感性引发了一个问题,即 ω3PUFA 饮食补充对胚胎发育和产前发育结果的不良影响。

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