cellular response to oxidative stress

Definition

Target type: biologicalprocess

Any process that results in a change in state or activity of a cell (in terms of movement, secretion, enzyme production, gene expression, etc.) as a result of oxidative stress, a state often resulting from exposure to high levels of reactive oxygen species, e.g. superoxide anions, hydrogen peroxide (H2O2), and hydroxyl radicals. [GOC:mah]

Cellular response to oxidative stress is a complex and multifaceted process that involves a coordinated effort by various cellular components to mitigate the damaging effects of reactive oxygen species (ROS). ROS are highly reactive molecules that can damage cellular components such as DNA, proteins, and lipids, leading to cellular dysfunction and ultimately cell death. To combat oxidative stress, cells have evolved a sophisticated network of defense mechanisms that include:

1. **Antioxidant enzymes:** These enzymes, such as superoxide dismutase (SOD), catalase, and glutathione peroxidase, catalyze the detoxification of ROS. SOD converts superoxide radicals into hydrogen peroxide, which is then broken down by catalase into water and oxygen. Glutathione peroxidase reduces hydrogen peroxide to water using reduced glutathione as a reducing agent.

2. **Non-enzymatic antioxidants:** These molecules, such as vitamins C and E, glutathione, and uric acid, can directly scavenge ROS. Vitamin C, also known as ascorbic acid, is a water-soluble antioxidant that can neutralize free radicals and regenerate other antioxidants. Vitamin E, a fat-soluble antioxidant, protects cell membranes from oxidative damage. Glutathione is a tripeptide that plays a crucial role in protecting cells from oxidative stress by reducing hydrogen peroxide and other ROS. Uric acid, a product of purine metabolism, can act as an antioxidant by scavenging free radicals.

3. **DNA repair mechanisms:** Oxidative damage to DNA can lead to mutations and cancer. Cells have evolved several DNA repair mechanisms to repair oxidative damage to DNA. These mechanisms include base excision repair (BER), nucleotide excision repair (NER), and mismatch repair (MMR).

4. **Protein repair mechanisms:** Oxidative stress can damage proteins by causing oxidation of amino acid side chains or fragmentation of the polypeptide chain. Cells have mechanisms to repair damaged proteins, such as the ubiquitin-proteasome system and chaperone proteins. The ubiquitin-proteasome system targets damaged proteins for degradation, while chaperone proteins can refold misfolded proteins.

5. **Signal transduction pathways:** Cells use various signaling pathways to respond to oxidative stress. These pathways often involve the activation of transcription factors, such as Nrf2, which induce the expression of antioxidant genes. Another important pathway involves the activation of MAP kinases, which can trigger apoptosis in response to severe oxidative stress.

6. **Induction of autophagy:** Autophagy is a process by which cells degrade and recycle damaged cellular components. Induction of autophagy can help cells to eliminate damaged organelles and proteins, thereby reducing the burden of oxidative stress.

The cellular response to oxidative stress is a dynamic process that is influenced by various factors, including the type and severity of the stress, the cell type, and the genetic background. Dysregulation of this complex network of defense mechanisms can contribute to the pathogenesis of various diseases, including cancer, cardiovascular disease, and neurodegenerative disorders. Understanding the mechanisms of cellular response to oxidative stress is crucial for developing therapeutic strategies to prevent and treat these diseases.'
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Proteins (37)

Compounds (1,387)