氧化应激及其在镉诱导的表观遗传学修饰中的作用:使用抗氧化剂作为一种可能的预防策略

E. Hernández-Cruz, Yalith Lyzet Arancibia-Hernández, Deyanira Yael Loyola-Mondragón, J. Pedraza-Chaverri
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引用次数: 5

摘要

氧化应激(OS)是镉等环境污染物引起毒性的主要机制之一。OS是一个自然的生理过程,其中氧化剂(如活性氧衍生物种(ROS))的存在超过了抗氧化防御策略,最终导致信号传导和氧化还原控制的中断。有人认为,镉主要通过诱导对电子传输链的损伤、增加烟酰胺腺嘌呤二核苷酸磷酸氢(NADPH)氧化酶(NOX)的活性和游离铁(Fe)的浓度以及降低抗氧化能力来增加ROS。另一方面,OS与表观基因组生物学的变化有关,会对健康产生不利影响。最近的研究表明,镉会改变脱氧核糖核酸(DNA)甲基化、组蛋白修饰和非编码RNA(ncRNA)的表达。然而,OS在Cd诱导的表观遗传学修饰中的作用仍然很少被探索。因此,本综述对OS的基本概念及其与Cd诱导的表观遗传学变化的关系进行了更新。此外,还提出使用抗氧化化合物来减轻镉诱导的表观遗传学改变。
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 and Its Role in Cd-Induced Epigenetic Modifications: Use of Antioxidants as a Possible Preventive Strategy
Oxidative stress (OS) represents one of the main mechanisms of toxicity induced by environmental pollutants such as cadmium (Cd). OS is a natural physiological process where the presence of oxidants, such as reactive oxygen-derived species (ROS), outweighs the strategy of antioxidant defenses, culminating in the interruption of signaling and redox control. It has been suggested that Cd increases ROS mainly by inducing damage to the electron transport chain and by increasing the activity of nicotinamide adenine dinucleotide hydrogen phosphate (NADPH) oxidase (NOX) and the concentration of free iron (Fe), as well as causing a decrease in antioxidant defense. On the other hand, OS has been related to changes in the biology of the epigenome, causing adverse health effects. Recent studies show that Cd generates alterations in deoxyribonucleic acid (DNA) methylation, histone modifications, and noncoding RNA (ncRNA) expression. However, the role of OS in Cd-induced epigenetic modifications is still poorly explored. Therefore, this review provides an update on the basic concepts of OS and its relationship with Cd-induced epigenetic changes. Furthermore, the use of antioxidant compounds is proposed to mitigate Cd-induced epigenetic alterations.
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