Arachidonic acid metabolism in skin: experimental contact dermatitis in guinea pigs.
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.
D000818:Animals; D001095:Arachidonic Acids / Q000378:metabolism*; D002855:Chromatography, Thin Layer; D003877:Dermatitis, Contact / Q000209:etiology / Q000276:immunology / Q000378:metabolism*; D004137:Dinitrochlorobenzene; D015237:Dinoprost; D015232:Dinoprostone; D005260:Female; D006168:Guinea Pigs; D008084:Lipoxygenase / Q000378:metabolism; D011457:Prostaglandins D / Q000378:metabolism; D011458:Prostaglandins E / Q000378:metabolism; D011460:Prostaglandins F / Q000378:metabolism; D012867:Skin / Q000276:immunology / Q000378:metabolism
D001095:Arachidonic Acids; D004137:Dinitrochlorobenzene; D011457:Prostaglandins D; D011458:Prostaglandins E; D011460:Prostaglandins F; D015237:Dinoprost; D008084:Lipoxygenase; D015232:Dinoprostone; C100006:prostaglandin F1