Oxidative Stress Response

Canonical source: Reactome R-HSA-3299685

Pathway Overview

The oxidative stress response encompasses enzymatic and non-enzymatic defenses against reactive oxygen species (ROS). Key enzymes include superoxide dismutases (SOD1, SOD2), catalase, glutathione peroxidases, and glutathione S-transferases (e.g., GSTP1). Nrf2 regulates many antioxidant genes. Air pollution, tobacco smoke, and UV radiation increase ROS; genetic variation in antioxidant enzymes modifies susceptibility to asthma, cardiovascular disease, and cancer. Tissue-specific expression and G×E are active research areas.

Environmental Triggers

Exposure	Trigger type
air-pollution	PM2.5 and ROS generation in airways
tobacco	Smoke-derived ROS and oxidative damage
uv-radiation	UV-induced ROS in skin

Genetic Modulation Points

Key genes

sod2— Mitochondrial superoxide dismutation
gstp1— Glutathione conjugation; detoxification

Tissue Specificity

No tissue specificity data recorded.

Disease Relevance

Linked diseases

asthma— G×E with air pollution; GSTP1, SOD2
coronary-artery-disease— Oxidative stress in endothelium

Linked exposures

air-pollution— PM2.5 induces ROS; antioxidant genes modify response
tobacco— Smoke increases ROS burden

Pathway Diagram

Pathway diagram placeholder. A visual representation of this pathway will be integrated when available.

Evidence Nodes

Evidence for this pathway is derived from:

3 environmental trigger(s)
2 key gene(s)
2 linked disease(s)
2 linked exposure(s)

References

1.Sies H, Jones DP (2020). Oxidative stress in disease and aging. Nature Reviews Molecular Cell Biology. doi:10.1038/s41580-020-00306-8
2.Islam T, et al. (2014). GSTP1 and air pollution–asthma associations. Environmental Health Perspectives. doi:10.1289/ehp.1307459