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金属、心血管风险以及与氧化应激的相互作用:一篇综述短文

Metals, cardiovascular risk, and the interplay with oxidative stress: a mini-review.

作者信息

Pires J G P, Schereider I R G, Cibin F W S, Scorza F A, Wiggers G A, Vassallo D V

机构信息

Curso de Medicina, Escola Superior de Ciências da Santa Casa de Misericórdia de Vitória - EMESCAM, Vitória, ES, Brasil.

Departamento de Ciências Fisiológicas, Centro de Ciências da Saúde, Universidade Federal do Espírito Santo, Vitória, ES, Brasil.

出版信息

Braz J Med Biol Res. 2025 Jun 20;58:e14466. doi: 10.1590/1414-431X2025e14466. eCollection 2025.

DOI:10.1590/1414-431X2025e14466
PMID:40561273
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12184964/
Abstract

Oxidative stress plays a key role in the mechanisms underlying pathophysiological processes, such as inflammation, age-related degenerative phenomena, atherosclerosis, hypertension, cancer, diabetes mellitus, neurodegenerative diseases, xenobiotic toxicity, among others. It is generated by the production of free radicals, resulting from the oxidative metabolism of cells. Oxidative stress is an important defense against infections. It acts specifically as a vasodilator and helps modulate antioxidant mechanisms. However, the effects become harmful when its production increases or antioxidant mechanisms are excessively reduced. Toxic metals from environmental and occupational exposure are silent agents that induce oxidative stress. Metals such as mercury (Hg), aluminum (Al), cadmium (Cd), and lead (Pb) are known to be toxic to various organs and tissues in our body. The present mini-review focuses on the cardiovascular system, considering that the interplay between oxidative stress and toxic metals acting silently is involved in their harmful effects, especially on the etiopathogenesis of cardiovascular disorders. A brief review is also given regarding the mechanisms of modulation of redox homeostasis by organic mechanisms, pharmacological approaches that can act directly or indirectly as antioxidants, and food-derived compounds that appear to be effective inhibitors of oxidative stress, thus preventing the harmful effects of free radicals.

摘要

氧化应激在多种病理生理过程的潜在机制中起着关键作用,如炎症、与年龄相关的退行性现象、动脉粥样硬化、高血压、癌症、糖尿病、神经退行性疾病、外源性物质毒性等。它是由细胞氧化代谢产生的自由基所引发的。氧化应激是抵御感染的重要防线。它具体发挥血管舒张剂的作用,并有助于调节抗氧化机制。然而,当氧化应激的产生增加或抗氧化机制过度减弱时,其影响就会变得有害。环境和职业接触中的有毒金属是引发氧化应激的隐匿因素。诸如汞(Hg)、铝(Al)、镉(Cd)和铅(Pb)等金属已知会对我们身体的各种器官和组织产生毒性。本综述聚焦于心血管系统,因为氧化应激与悄然起作用的有毒金属之间的相互作用涉及其有害影响,尤其是在心血管疾病的发病机制方面。此外,还简要回顾了通过有机机制调节氧化还原稳态的机制、可直接或间接作为抗氧化剂起作用的药理学方法,以及似乎是氧化应激有效抑制剂的食物衍生化合物,从而预防自由基的有害影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ec4/12184964/3a9be6b56396/1414-431X-bjmbr-58-e14466-gf001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ec4/12184964/3a9be6b56396/1414-431X-bjmbr-58-e14466-gf001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ec4/12184964/3a9be6b56396/1414-431X-bjmbr-58-e14466-gf001.jpg

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本文引用的文献

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Growth differentiation factor-15, a novel systemic biomarker of oxidative stress, inflammation, and cellular aging: Potential role in cardiovascular diseases.生长分化因子-15,一种氧化应激、炎症和细胞衰老的新型全身生物标志物:在心血管疾病中的潜在作用。
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Chronic exposure to mercury increases arrhythmia and mortality post-acute myocardial infarction in rats.
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