Abstract

The cutaneous metabolism of exogenous arachidonic acid and endoperoxide (PGH2) to prostaglandins and hydroxy-fatty acids was investigated in experimental contact dermatitis in guinea pigs and compared to normal skin, unsensitized animals treated with the allergen dinitrochlorobenzene, and Trafuril-induced irritant dermatitis. The main alterations of cutaneous arachidonate metabolism in contact dermatitis comprise: (1) an inhibition of PGD2 synthesis; (2) a switch from predominant PGD2 production to a predominance of PGE2 and (3) a marked inhibition of the lipoxygenase activity.

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