Increased biosynthesis of lipoxygenase products by UVB-irradiated guinea pig epidermis: evidence of a cyclooxygenase inhibitor.

The present studies demonstrate that incubation of arachidonic acid (AA) with a 20,000 g homogenate (containing both microsomal and cytoplasmic fractions) from UVB-irradiated guinea pig epidermis (24-72 h) resulted in decreased transformation of the [14C]AA into the cyclooxygenase products (PGD2, PGE2, and PGF2 alpha) while the incorporation of 14C into lipoxygenase products (15-HETE and 12-HETE) increased. An investigation into the selective inhibition of the cyclooxygenase pathway revealed that the in vitro transformation of [14C]AA into [14C]-cyclooxygenase products by the 100,000 g particulate fraction prepared from normal unirradiated guinea pig epidermis was inhibited by the 100,000 g cytoplasmic extract prepared from a 24-h postirradiated guinea pig epidermis. These latter data imply that an endogenous inhibitor of the cyclooxygenase pathway is generated and released into the cytoplasm during UVB irradiation and it is likely that this selective inhibition of the cyclooxygenase pathway may contribute at least in part to the increased lipoxygenase products in the 24-h postirradiated skin specimens and possibly the recognized prolonged UVB-induced inflammatory process.