Hydrogen sulfide, endoplasmic reticulum stress and alcohol mediated neurotoxicity.
Hydrogen sulfide, endoplasmic reticulum stress and alcohol mediated neurotoxicity.
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DOI：
10.1016/j.brainresbull.2017.02.002
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发表时间：
2017-04
影响因子：
3.8
通讯作者：
Tyagi N
中科院分区：
文献类型：
--
作者：
George AK;Behera J;Kelly KE;Zhai Y;Tyagi N
酒精是现代社会中最被社会接受的成瘾性药物之一。它的滥用影响到几乎所有的器官系统，中枢神经系统（CNS）特别容易受到过量酒精暴露的影响。酒精暴露也会对成年人和发育中的大脑造成严重损害。过量的酒精消费会引起许多病理生理应激反应，其中之一是内质网（ER）应激反应。引发酒精诱导的内质网应激反应的潜在机制与酒精代谢直接或间接相关，包括乙醛和同型半胱氨酸的毒性水平、氧化应激和异常表观遗传修饰。越来越多的证据表明，H2S是最新认识的气体递质，对氧化应激诱导的神经毒性具有巨大的生理保护功能。在这篇综述中，我们解决了酒精诱导的氧化应激介导的内质网应激和H2S在其缓解酒精神经毒性的背景下的作用。预期ER应激触发物的中断对酒精介导的疾病和病症具有治疗益处。
Alcohol is one of the most socially accepted addictive drugs in modern society. Its abuse affects virtually all organ systems with the central nervous system (CNS) being particularly vulnerable to excessive alcohol exposure. Alcohol exposure also causes profound damage to both the adult and developing brain. Excessive alcohol consumption induces numerous pathophysiological stress responses, one of which is the endoplasmic reticulum (ER) stress response. Potential mechanisms that trigger the alcohol induced ER stress response are either directly or indirectly related to alcohol metabolism, which include toxic levels of acetaldehyde and homocysteine, oxidative stress and abnormal epigenetic modifications. Growing evidence suggests that H2S is the most recently recognized gasotransmitter with tremendous physiological protective functions against oxidative stress induced neurotoxicity. In this review we address the alcohol induced oxidative stress mediated ER stress and the role of H2S in its mitigation in the context of alcohol neurotoxicity. Interruption of ER stress triggers is anticipated to have therapeutic benefits for alcohol mediated diseases and disorders.
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影响因子：
37.8
作者：
Calvert JW;Elston M;Nicholson CK;Gundewar S;Jha S;Elrod JW;Ramachandran A;Lefer DJ
通讯作者：
Lefer DJ
硫化氢可减轻小鼠中脑内施用的同型半胱氨酸诱导的神经变性和神经血管功能障碍。
影响因子：
3.3
作者：
Kamat PK;Kalani A;Givvimani S;Sathnur PB;Tyagi SC;Tyagi N
通讯作者：
Tyagi N
影响因子：
4.7
作者：
Ho, PI;Collins, SC;Shea, TB
通讯作者：
Shea, TB
影响因子：
4.8
作者：
Kimura, Y;Kimura, H
通讯作者：
Kimura, H
影响因子：
14.5
作者：
den Heijer, T;Vermeer, SE;Breteler, MMB
通讯作者：
Breteler, MMB