Hydrogen Sulfide, Endoplasmic Reticulum Stress and Alcohol Mediated Neurotoxicity

Overview

Journal Brain Res Bull

Specialty Neurology

Date 2017 Feb 19

PMID 28212849

Citations 8

Authors

Akash K George

Jyotirmaya Behera

Kimberly E Kelly

Yuankun Zhai

Neetu Tyagi

Affiliations

Soon will be listed here.

Abstract

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 HS 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 HS 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.

Citing Articles

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