Mitochondrial Stress by Toxic Elements - An Overview

Rana Svs
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引用次数: 1

Abstract

Mitochondria (mT) are now considered as suitable targets of toxicity induced by various environmental xenobiotics. Mitochondrial dysfunction is the final outcome of their effects in cellular system. Human diseases viz. Alzheimer, parkinsonism, pancreatic β cell failure, insulin resistance and ageing have also been partially attributed to mitochondrial injury. Present review focuses mainly on mitochondrial stress induced by a few toxic elements i.e. cadmium, mercury, lead, copper, chromium, nickel and arsenic. General mechanisms that cause mT dysfunction including generation of reactive oxygen species, oxidative stress, apoptosis alterations in mT membrane permeability and energy disturbances have been discussed. Further, specific effects of toxic elements i.e. inhibition of ATPase, activation of caspases, enhanced release of cytochrome c and mT DNA damage have also been described. In few cases, cytokines were also involved in mT dysfunction. Their effects on mT biogenesis is also reported. Investigations on certain less understood paradigms viz. mitochondrial hormesis, mitophagy and mitokines are urgently needed.
线粒体应激有毒元素-概述
线粒体(mT)目前被认为是各种环境外源物诱导的毒性的合适靶点。线粒体功能障碍是其作用于细胞系统的最终结果。人类疾病,如阿尔茨海默病、帕金森病、胰腺β细胞衰竭、胰岛素抵抗和衰老也部分归因于线粒体损伤。目前的研究主要集中在镉、汞、铅、铜、铬、镍和砷等几种有毒元素引起的线粒体应激。引起mT功能障碍的一般机制包括活性氧的产生、氧化应激、mT膜通透性的凋亡改变和能量干扰。此外,有毒元素的特定作用,即ATPase的抑制,半胱天冬酶的激活,细胞色素c的释放增强和mT DNA损伤也被描述。在少数情况下,细胞因子也参与mT功能障碍。它们对mT生物发生的影响也有报道。目前迫切需要对线粒体激效、线粒体自噬和线粒体因子等一些不太了解的范式进行研究。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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