Cyclosporin A inhibits biological effects of tumor promoting phorbol esters.
The antilymphocytic and antiphlogistic agent cyclosporin A (CsA) inhibits in vivo various effects induced by the tumor promoting phorbol ester 12-0-tetradecanoylphorbol-13-acetate (TPA). These include the edema of the mouse ear, the alkaline phosphatase (AP) activity and the ornithine decarboxylase (ODC) activity in mouse epidermis as well as the generation of a specific arachidonic acid (AA) metabolite in mouse epidermis. AA metabolism in an epidermal cell-free system of mouse epidermis was not suppressed by CsA. According to thin layer chromatography the TPA-induced and as yet unidentified AA metabolite exhibits a polarity between that of 5-HETE and 12-/15-HETE. Studies with inhibitors indicate it to be a lipoxygenase product.
D000818:Animals; D016718:Arachidonic Acid; D001095:Arachidonic Acids / Q000378:metabolism; D002471:Cell Transformation, Neoplastic / Q000187:drug effects*; D002855:Chromatography, Thin Layer; D003524:Cyclosporins / Q000494:pharmacology*; D004487:Edema / Q000139:chemically induced; D005260:Female; D051379:Mice; D010704:Phorbols / Q000037:antagonists & inhibitors*; D012867:Skin / Q000187:drug effects / Q000378:metabolism; D013755:Tetradecanoylphorbol Acetate / Q000037:antagonists & inhibitors*; D013997:Time Factors
D001095:Arachidonic Acids; D003524:Cyclosporins; D010704:Phorbols; D016718:Arachidonic Acid; D013755:Tetradecanoylphorbol Acetate