Reactive oxygen species (oxyradicals) are continually produced in biological systems as unwanted toxic bi-products of normal metabolism. Oxyradical production can be increased by interaction with foreign chemicals (xenobiotics) through various processes involving components of the mixed-function oxygenase (MFO) system, including enzyme induction and redox cycling. Failure to remove and detoxify oxyradicals by antioxidant defences can lead to biological damage. Antioxidant enzymes (superoxide dismutase, catalase, glutathione peroxidase) and free radical scavengers (vitamins C and E, carotenoids, glutathione) are widespread in marine organisms, and generally present in highest levels in the major tissue localization of the MFO system and the site of organic xenobiotic metabolism, such as the liver of fish and digestive gland of bivalve molluscs. The antioxidant enzymes DT-diaphorase and aldehyde dehydrogenase, which are part of the [Ah]-gene battery in mammals, are also indicated to be widespread in fish, but little is known of their properties or function. Mechanistic studies of flounder (P.ƒlesus) and mussel (M. edulis) indicate that microsomal oxyradical production can be stimulated by a wide range of xenobiotics via redox cycling (nitroaromatics, quinones) and other free radical interactions (pesticides). These xenobiotics include both the pollutants themselves (e.g. quinones in pulp mill effluents) and their metabolic products (e.g. benzo[a]pyrene-diones). Inhibitor studies indicate the involvement of cytochrome P450 reductase in redox cycling in flounder liver. Microsomal dione production from benzo[a]pyrene is much greater in mussel than flounder, but is greatly increased in the latter by the hydroperoxide-dependent peroxidase activity of cytochrome P450. Lipid peroxidation is increased in fish by exposure to xenobiotics, indicating the possibility of an aromatic hydrocarbon-mediated toxic cycle of oxyradical generation leading to lipid peroxidation, leading to increased production of redox cycling diones, leading finally to increased oxyradical production and further biological damage.