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Imbalanced GSH/ROS and sequential cell death.

Ting Liu¹, Li Sun^2,3, Yubin Zhang^2,3

¹State Key Laboratory of Functions and Applications of Medicinal Plants, Guizhou Provincial Key Laboratory of Pharmaceutics, Guizhou Medical University, Guiyang, China.

Journal of Biochemical and Molecular Toxicology

|November 2, 2021

Summary

This summary is machine-generated.

Cellular metabolism generates reactive oxygen species (ROS), which can deplete glutathione (GSH). This imbalance disrupts cellular functions, leading to cell death.

Keywords:

GSH ROS apoptosis redox balance stress signaling pathways

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Area of Science:

Biochemistry
Cell Biology

Background:

Cellular metabolism naturally produces reactive oxygen species (ROS).
Glutathione (GSH) is a key biomolecule involved in antioxidant defense, free radical scavenging, and electrophile elimination.
An imbalance between ROS and GSH can lead to oxidative damage and cell death.

Purpose of the Study:

To review the occurrence and consequences of ROS/GSH imbalance.
To identify factors that disrupt the cellular ROS/GSH balance.
To discuss how this imbalance leads to cell death.

Main Methods:

Literature review using keywords "GSH" and "ROS".

Main Results:

Excessive ROS can react with vital biomolecules like DNA, RNA, proteins, and GSH.
Disruption of the ROS/GSH balance causes oxidation and chemical modification of biomacromolecules.
Factors contributing to imbalance include increased ROS, GSH consumption, and interference with oxidoreductase or thioredoxin activity.
Chemicals like arsenic trioxide (ATO), pyrogallol (PG), and MG132 can disrupt ROS/GSH balance.

Conclusions:

Imbalanced ROS/GSH homeostasis is detrimental to cells.
This imbalance results in cell-cycle arrest, proliferation inhibition, and ultimately cell death.
Understanding the factors disrupting ROS/GSH balance is crucial for comprehending cell death pathways.