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.