Retinoids activate superoxide production by polymorphonuclear leucocytes.
Retinol and retinoic acid were effective activators of oxygen consumption by human polymorphonuclear leucocytes (PMN) in micromolar concentrations. In contrast, retinyl acetate was ineffective as an activator. Retinol caused activation only after a lag time, the length of which depended on retinol concentration. Oxygen consumption was due to superoxide production by PMN. Superoxide production was observed as superoxide dismutase-inhibitable cytochrome c reduction. Previously, retinoids have been reported to inhibit PMN activation by phorbol myristate acetate, a tumour promoter. This retinoid-induced inhibition of PMN activation has been suggested to be a mechanism by which retinoids may protect against carcinogenesis in animals. However, the retinoid concentrations at which PMN inhibition was reported were much higher than those found to cause activation in this study. We found that retinoic acid slightly inhibited phorbol myristate acetate-activated superoxide production, but only at concentrations that caused activation. In contrast, activation by formyl-Met-Leu-Phe was effectively inhibited at a retinoic acid concentration that did not cause activation by itself.
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D004224:Diterpenes; D005033:Ethylmaleimide / Q000494:pharmacology; D006801:Humans; D009504:Neutrophils / Q000187:drug effects*; D010101:Oxygen Consumption / Q000187:drug effects*; D012176:Retinoids / Q000494:pharmacology*; D000084562:Retinyl Esters; D013482:Superoxide Dismutase / Q000494:pharmacology; D013481:Superoxides / Q000378:metabolism*; D013997:Time Factors; D014212:Tretinoin / Q000494:pharmacology; D014801:Vitamin A / Q000031:analogs & derivatives / Q000494:pharmacology
D004224:Diterpenes; D012176:Retinoids; D000084562:Retinyl Esters; D013481:Superoxides; D014801:Vitamin A; C009166:retinol acetate; D014212:Tretinoin; D013482:Superoxide Dismutase; D005033:Ethylmaleimide