Reactive oxygen species (ROS) are short lived, highly reactive molecules derived from oxygen, such as superoxide, hydrogen peroxide and hydroxyl radicals. They are produced continuously in cells, mainly by the mitochondrial electron transport chain, as well as by enzymes like NADPH oxidases, xanthine oxidase and various oxidases in peroxisomes and the endoplasmic reticulum.

Research has shifted from viewing ROS only as damaging agents to recognizing their dual role. At high concentrations, ROS oxidize DNA, proteins and lipids, contributing to mutagenesis, cell death, aging and diseases such as cancer, neurodegeneration, cardiovascular disorders and diabetes. Oxidative stress arises when ROS production overwhelms antioxidant defenses, which include enzymatic systems such as superoxide dismutases, catalase, glutathione peroxidases and peroxiredoxins, along with non enzymatic antioxidants like glutathione, vitamins C and E and carotenoids.

At controlled, moderate levels, ROS act as signaling molecules that regulate processes such as cell proliferation, differentiation, immune responses and adaptation to stress. They modulate signaling pathways by reversible oxidation of cysteine residues in proteins, influencing kinase and phosphatase activity, transcription factors and ion channels. Cells tune ROS signaling spatially and temporally, for example through specialized NADPH oxidase complexes that generate ROS in specific compartments.

A key current theme is redox homeostasis, the dynamic balance between ROS generation and antioxidant capacity. Disruption of this balance is linked to pathology, yet excessive antioxidant supplementation can blunt essential ROS signaling. Ongoing research aims to develop targeted redox based therapies that adjust ROS levels in precise cellular locations rather than simply eliminating them.