Reactive oxygen species (ROS) are chemically reactive, oxygen-containing chemical species that are generated as byproducts of cellular metabolism. In animal cells, generation of ROS typically occurs in the mitochondria. In plant cells, ROS can also be generated in chloroplasts. More recently, ROS has been shown to be generated in peroxisomes and from plasma membrane oxidases of various cell types.

When generated in excess, ROS has long been thought to result in damage of cellular macromolecules such as DNA, lipids and proteins. Holistically, this is represented by a cell's oxidative stress state. Such states of stress have been linked to cellular processes such as apoptosis, and more macroscopically, play a role in the pathogenesis of many human diseases.

Because of its damaging effects, cells have several carefully regulated systems for managing excess ROS. The most well studied system is the glutathione-ascorbate cycle, which detoxifies H₂O₂ into H₂O, using NADH and NADPH as electron donors. Other systems include enzymes such as superoxide dismutase, which catalyzes the dismutation of the superoxide anion (O₂^-) into O₂ or H₂O₂, and catalase, which catalyzes the decomposition of H₂O₂ into H₂O and O₂.

While ROS has been extensively studied for their detrimental effect on cells, it is only more recently that studies have looked at the role of ROS in cell signaling. In controlled amounts, ROS has been shown to regulate gene activation. The specific mechanism by which this occurs is, however, still up for debate. It is possible that ROS binds to special receptors which initiate a signaling cascade leading up to gene regulation. It is also possible that ROS directly modifies the proteins in such a signaling cascade, perhaps by regulation of protein phosphorylation.

Due to its importance in biological systems, a plethora of tools have been developed to study ROS both in vitro and in vivo. The table below provides a summary of the most common tools as well as their targets.