redoxhomeostas

Redox homeostasis refers to the cellular and organismal maintenance of a balanced redox state, ensuring that reactive oxygen and nitrogen species are kept at levels that support function without causing damage. It integrates antioxidant defenses with controlled redox signaling, recognizing that some ROS and RNS act as signaling molecules rather than solely as harmful byproducts.

Key components include redox couples such as NAD+/NADH, NADP+/NADPH, and the glutathione system (GSH/GSSG). These reservoirs of reducing equivalents participate in metabolism, repair, and the regulation of protein activity through reversible oxidation of cysteine residues. Antioxidant defenses comprise enzymatic systems—superoxide dismutase, catalase, glutathione peroxidases, peroxiredoxins, and the thioredoxin/glutaredoxin networks—and nonenzymatic antioxidants such as glutathione and vitamins C and E.

Redox signaling arises from controlled ROS/RNS production, notably from mitochondria and NADPH oxidases, which modulate transcription factors and enzymes to influence processes like proliferation, differentiation, autophagy, and inflammatory responses. The balance is dynamic and stimuli-dependent, and disturbances can shift toward oxidative stress, implicated in aging and various diseases, or toward reductive stress if reductive capacity becomes excessive.

Measurement and study rely on indicators such as GSH/GSSG and NAD+/NADH ratios, redox-sensitive probes, and redox proteomics to detect reversible post-translational modifications. Therapeutically, strategies aim to modulate redox pathways or support endogenous defenses rather than indiscriminately suppress ROS, reflecting the nuanced role of redox biology in health and disease.