Journal
JOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY
Volume 36, Issue 1, Pages -Publisher
WILEY
DOI: 10.1002/jbt.22942
Keywords
apoptosis; GSH; redox balance; ROS; stress signaling pathways
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Funding
- National Natural Science Foundation of China [81760699, 82060703, U1812403-05]
- Guizhou Provincial Natural Science Foundation [[2019]1280]
- Guizhou Education Department [KY[2021]033]
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This article reviews the impact of imbalance between ROS and GSH on cells, indicating that imbalance may lead to cell death. In addition, different factors leading to the disruption of cellular ROS and GSH balance are introduced.
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.
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