The inflammation produced by exposure to ultraviolet (UV) light has been well documented clinically and histologically. However, the mechanisms by which mediators induce this clinical response remain poorly defined. It is clear that photochemistry occurring after UV absorption must be responsible for initiating these events. Some of these underlying mechanisms have been defined. After exposure to UV light, the formation of prostaglandins and the release of histamine are increased. In addition to an increase in the quantity of these mediators, an increase in sensitivity of irradiated tissue to agonist stimulation also occurs. This increased sensitivity may cause tissue to respond to agonist levels previously present. Phospholipase activity also increases, making more substrate available for prostaglandin formation. Oxygen radical-induced peroxidation of membrane lipids caused by irradiation may contribute to increased phospholipase activity. Oxygen-free radicals also participate in sunburn cell formation and in UV-induced decreases in Langerhans cell numbers. Several enzymatic and non-enzymatic mechanisms are present in skin for reducing these highly reactive oxygen species.