Δ133p53 Functions to Maintain Redox Homeostasis in Response to Low ROS Stresses

Reactive oxygen species (ROS) including superoxide anion (O2•-), hydroxyl radical (OH•) and non-radical species hydrogen peroxide (H2O2) are generated during mitochondrial oxidative metabolism and as a cellular response to xenobiotics and bacterial invasion in aerobic organisms. Moderate levels of ROS can function as signals that promote cell growth and division. However, when overproduced, ROS overwhelm a cell’s capacity to maintain redox homeostasis, and can cause oxidative stress, which results in the oxidation of macromolecules such as proteins, membrane lipids and mitochondria or genomic DNA. The detrimental accumulation of ROS eventually leads to abnormal cell death and senescence, which contributes to the development of neurodegenerative diseases, cancer, and aging-related pathologies.

Δ133p53 Functions
Δ133p53 Functions

To maintain redox homeostasis, organisms have evolved with numerous endogenous antioxidant defense systems including both enzymatic and non-enzymatic antioxidant mechanisms that can either scavenge ROS or prevent their formation. Tumour repressor p53 plays important and complex roles in response to oxidative stress.

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