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辅酶Q10与外源化学物代谢:概述

Coenzyme Q10 and Xenobiotic Metabolism: An Overview.

作者信息

Mantle David, Golomb Beatrice A

机构信息

Pharma Nord (UK) Ltd., Morpeth NE61 2DB, Northumberland, UK.

San Diego School of Medicine, University of California, La Jolla, CA 92093, USA.

出版信息

Int J Mol Sci. 2025 Jun 17;26(12):5788. doi: 10.3390/ijms26125788.

Abstract

Mitochondria are primary targets for environmental toxic chemicals; these typically disrupt the mitochondrial electron transport chain, resulting in reduced ATP production, increased reactive oxygen free radical species (ROS)-induced oxidative stress, increased apoptosis, and increased inflammation. This in turn suggests a rationale for investigating the potential role of coenzyme Q10 (CoQ10) in mediating such chemical-induced mitochondrial dysfunction, given the key roles of CoQ10 in promoting normal mitochondrial function, and as an antioxidant and anti-apoptotic and anti-inflammatory agent. In the present article, we have, therefore, reviewed the potential role of supplementary CoQ10 in improving mitochondrial function and mediating adverse effects following exposure to a number of environmental toxins, including pesticides, heavy metals, industrial solvents, endocrine-disrupting agents, and carcinogens, as well as pharmacological drugs and lifestyle toxicants.

摘要

线粒体是环境有毒化学物质的主要作用靶点;这些物质通常会破坏线粒体电子传递链,导致三磷酸腺苷(ATP)生成减少、活性氧自由基(ROS)诱导的氧化应激增加、细胞凋亡增加以及炎症加剧。鉴于辅酶Q10在促进线粒体正常功能方面的关键作用,以及作为抗氧化剂、抗凋亡和抗炎剂的作用,这进而为研究辅酶Q10在介导此类化学物质诱导的线粒体功能障碍中的潜在作用提供了理论依据。因此,在本文中,我们综述了补充辅酶Q10在改善线粒体功能以及介导暴露于多种环境毒素(包括农药、重金属、工业溶剂、内分泌干扰物和致癌物)、药理药物和生活方式毒物后产生的不良反应方面的潜在作用。

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