Eicosanoids in skin UV inflammation.

Several studies have implicated the eicosanoids as mediator substances in different types of UV inflammation. In human UV erythema, various arachidonic acid metabolites--mainly cyclooxygenase products--have been detected, particularly in skin exudates. The concentration and the sequence of release of the various eicosanoids vary in relation to the time course and the various types of UV-induced erythema. UVB, UVC but not UVA erythema at its maximum was only to some extent inhibited by indomethacin despite almost complete inhibition of the synthesis of prostaglandins E2 and F2 alpha. A major issue cannot, as yet, be answered satisfactorily: are one or a number of eicosanoids per se causing the erythema or are they only passive bystanders released by damage to cellular structures? Until further evidence has been provided, the causative role of E and F prostaglandins in relation to development of UV erythema is doubtful. By contrast, PGI2 is a more likely candidate in this respect, being synthesized and released close to the events occurring in the vessel walls. The lipoxygenase pathway is still too unexplored for proper evaluation with regard to a role in the pathogenesis, but the pharmacological properties of leukotrienes and hydroxy-fatty acids may qualify them as potential candidates alone or in a concert of mediator events occurring during the developments of UV inflammation.