Possible mechanisms for induction of oxidative stress and suppression of systemic nitric oxide production caused by exposure to environmental chemicals.
Possible mechanisms for induction of oxidative stress and suppression of systemic nitric oxide production caused by exposure to environmental chemicals.
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DOI：
10.1007/bf02897942
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发表时间：
2002-09-01
影响因子：
4.7
通讯作者：
Shimojo, Nobuhiro
中科院分区：
文献类型：
--
作者：
Kumagai, Yoshito;Shimojo, Nobuhiro
暴露于具有亲电特性的环境化学物质引起的细胞毒性效应通常归因于通过巯基或酶介导的氧化还原循环与细胞内大分子共价连接，导致活性氧（ROS）的产生。当大量的活性氧形成时，它们会压倒抗氧化防御，导致氧化应激的诱导。一氧化氮 (NO) 在血管张力中起着至关重要的作用，由内皮一氧化氮合酶 (eNOS) 形成。由于全身 NO 产生的减少与血管疾病的病理生理作用有关，因此环境化学物质导致的 eNOS 功能障碍与心肺相关疾病和死亡有关。在这篇综述中，我们介绍了亲电子试剂基于机制的毒性（共价连接和氧化还原循环）。因此，本综述将重点关注环境化学物质引起氧化应激和NO生成受损的可能机制。
The cytotoxic effects evoked by exposure to environmental chemicals having electrophilic properties are often attributable to covalent attachment to intracellular macromolecules through sulfhydryl groups or enzyme-mediated redox cycling, leading to the generation of reactive oxygen species (ROS). When huge amounts of ROS form they overwhelm antioxidant defenses resulting in the induction of oxidative stress. Nitric oxide (NO) which plays a crucial role in vascular tone, is formed by endothelial NO synthase (eNOS). Since a decrease in systemic NO production is implicated in the pathophysiological actions of vascular diseases, dysfunction of eNOS by environmental chemicals is associated with cardiopulmonary-related diseases and mortality. In this review, we introduce the mechanism-based toxicities (covalent attachment and redox cycling) of electrophiles. Therefore, this review will focus on the possible mechanisms for the induction of oxidative stress and impairment of NO production caused by environmental chemicals.