Back to Search Start Over

Imbalanced GSH/ROS and sequential cell death.

Authors :
Liu, Ting
Sun, Li
Zhang, Yubin
Wang, Yonglin
Zheng, Jiang
Source :
Journal of Biochemical & Molecular Toxicology; Jan2022, Vol. 36 Issue 1, p1-9, 9p
Publication Year :
2022

Abstract

Reactive oxygen species (ROS) are produced in cells during metabolic processes. Excessive intracellular ROS may react with large biomolecules, such as DNA, RNA, proteins, and small biomolecules, that is, glutathione (GSH) and unsaturated fatty acids. GSH has physiological functions, including free radical scavenging, anti‐oxidation, and electrophile elimination. The disruption of ROS/GSH balance results in the deleterious oxidation and chemical modification of biomacromolecules, which eventually leads to cell‐cycle arrest and proliferation inhibition, and even induces cell death. Imbalanced ROS/GSH may result from a direct increase of ROS, consumption of GSH, intracellular oxidoreductase interference, or thioredoxin activity reduction. Some chemicals including arsenic trioxide (ATO), pyrogallol (PG), and carbobenzoxy‐Leu‐Leu‐leucinal (MG132) could also disrupt the balance of GSH and ROS. This article reviews the occurrence and consequences of the imbalance between GSH and ROS and introduces factors responsible for the disruption of cellular ROS and GSH balance, resulting in cell death. "GSH" and "ROS" were used as keywords to search the relevant literaturess. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
10956670
Volume :
36
Issue :
1
Database :
Complementary Index
Journal :
Journal of Biochemical & Molecular Toxicology
Publication Type :
Academic Journal
Accession number :
154758701
Full Text :
https://doi.org/10.1002/jbt.22942