氧化应激、线粒体功能障碍与神经退行性疾病:综述

Shalini K. Sawhney
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摘要

摘要:氧化应激是由活性氧/氮(ROS/RNS)产生的,涉及线粒体功能障碍。线粒体是氧化应激的主要来源之一,因为它利用氧气来产生能量。ROS的过量产生会导致氧化应激,从而损害细胞结构、脂质、蛋白质和DNA。与许多疾病相关的各种氧化事件是由于氧化应激引起的,包括线粒体蛋白、线粒体脂质和线粒体DNA的改变,这反过来导致神经细胞损伤,因为它们的代谢非常活跃。中等浓度的活性氧/氮还在许多正常生理过程中发挥作用,如信号传导途径、诱导有丝分裂反应和防御感染性病原体。氧化应激一直被认为是神经退行性疾病的主要病因,包括帕金森病(PD)和阿尔茨海默病(AD)。近年来对帕金森病相关基因功能障碍和功能的研究,为了解与疾病过程相关的生化途径提供了新的基础。本文综述了自由基产生的来源、线粒体功能障碍以及帕金森病和阿尔茨海默病相关的神经退行性疾病的机制。这使得线粒体成为PD和AD研究的主要目标。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Oxidative stress, Mitochondrial dysfunction and Neuro-degenerative diseases: A Review
http://dx.doi.org/10.21276/IJRDPL.22780238.2019.8(1).1-5 ABSTRACT: Oxidative stress is produced by the reactive oxygen/nitrogen species (ROS/RNS) which involves mitochondrial dysfunction. Mitochondria is one of the main sources of oxidative stress, as it utilizes the oxygen for the energy production. Overproduction of ROS, results in oxidative stress, which injures the cell structures, lipids, proteins, and DNA. Various oxidative events implicated in many diseases is due to oxidative stress which include alteration in mitochondrial proteins, mitochondrial lipids and mitochondrial DNA, which in turn leads to damage nerve cells as they are metabolically very active. Reactive oxygen/nitrogen species at moderate concentrations also play roles in normal physiology of many processes like signalling pathways, induction of mitogenic response and in defence against infectious pathogens. Oxidative stress has been considered to be the main cause in the etiology of neurodegenerative diseases, which includes Parkinson’s disease (PD) and Alzheimer’s disease (AD). Recent research on the dysfunction and function of PD associated genes has provided new fundamental insights into biochemical pathways that are linked with the disease process This review includes source of free radical generation, mitochondrial dysfunction and the mechanism involved in neurodegenerative diseases which involves both PD as well as in AD. This makes the mitochondria, the main target of PD and AD research.
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