Abstract
Abstract
This study has demonstrated that exposure of white domestic pig skin to a single treatment of X-ray irradiation (300-1000 rad) results in a rapid release of epidermal arachidonic acid followed by its transformation via the cyclooxygenase pathway into prostaglandin E2 (PGE2). Beyond 24 hr the epidermal PGE2 decreased steadily. The time-dependent biosynthesis of epidermal PGE2 can be blocked by the immediate topical application of 2.5% indomethacin in ethanol to the irradiated skin area. In order to seek an explanation for the progressive decrease of epidermal PGE2 beyond 24 hr we assayed for the activity of the NADPH-dependent PGE2-9-ketoreductase (an enzyme which catalyzes the transformation of PGE2 into PGF2α in the 105,000g supernatant fractions prepared from the irradiated and nonirradiated epidermal specimens. Our data revealed that the activity of this interconverting enzyme increased steadily beyond 24 hr. These results indicate that PGE2 formed as a result of exposure of skin to X-rays is metabolized into PGF2α. The biological significance of this interconversion and the role of PGF2a in X-ray-induced injury to the skin remains to be determined.
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