ABSTRACT
Avast number of experimental and clinical studies implicates oxygen-derived free radicals(especially, superoxide and hydroxyl radical) and high energy oxidants (such asperoxynitrite) as mediators of acute and chronic inflammation. The purpose of this review is to describe the role of endogenous and exogenous melatonin in inflammation. Reactive oxygen species can modulate a wide range of toxic oxidative reactions. These include initiation of lipid peroxidation, direct inhibition of mitochondrial respiratory chain enzymes, inactivation of glyceraldehyde-3phosphate dehydrogenase, inhibition of membrane sodium/ potassium ATP-ase activity, inactivation of membrane sodium channels, and other oxidative modifications of proteins. Reactive oxygen species (e.g., superoxide, peroxynitrite, hydroxyl radical and hydrogen peroxide) are all potential reactants capable of initiating DNA single strand breakage, with subsequent activation of the nuclear enzyme poly (ADP ribose) synthetase (PARS), leading to eventual severe energy depletion of the cells, and necrotic-type cell death. All these toxicities are likely to play a role in the pathophysiology of inflammation. Melatonin has been shown to posses in vitro an important antioxidant capacity as well as to inhibits the activation of poly (ADP ribose) synthetase. Therefore a large number of experimental studies have demonstrated that melatonin may exert an important anti-inflammatory action.
