Dehydroepiandrosterone and 16 alpha-Br-epiandrosterone inhibit 12-O-tetradecanoylphorbol-13-acetate stimulation of superoxide radical production by human polymorphonuclear leukocytes.
Both dehydroepiandrosterone (DHEA) and the synthetic steroid 16 alpha-Br-epiandrosterone (Br-Epi), a more potent inhibitor of glucose-6-phosphate dehydrogenase (G6PDH) than DHEA, inhibit the 12-O-tetradecanoylphorbol-13-acetate (TPA) stimulation of superoxide anion (O2-) formation by human neutrophils. DHEA has previously been shown to inhibit the development of spontaneous breast cancer and chemically induced tumors of the lung and colon as well as TPA promoted skin tumors in the mouse. The inhibition of TPA stimulated O2- formation by DHEA may contribute to the cancer preventive activity of this steroid.
Whitcomb
J M
JM
Schwartz
A G
AG
D000738:Androsterone / Q000031:analogs & derivatives* / Q000494:pharmacology; D003687:Dehydroepiandrosterone / Q000494:pharmacology*; D005609:Free Radicals; D005954:Glucosephosphate Dehydrogenase / Q000037:antagonists & inhibitors; D006801:Humans; D066298:In Vitro Techniques; D009504:Neutrophils / Q000378:metabolism*; D010704:Phorbols / Q000633:toxicity*; D013481:Superoxides / Q000378:metabolism*; D013755:Tetradecanoylphorbol Acetate / Q000633:toxicity*
D005609:Free Radicals; D010704:Phorbols; D013481:Superoxides; C032020:16-bromoepiandrosterone; D003687:Dehydroepiandrosterone; D000738:Androsterone; D005954:Glucosephosphate Dehydrogenase; D013755:Tetradecanoylphorbol Acetate