Flavonoids are plant-based phenolic compounds, and quercetin is the most abundant dietary member of this family. One of the most important characteristics of quercetin is its antioxidant property. The aim of this study was to investigate antioxidant effects of quercetin on corpora cavernosa of mice. Corpora cavernosa were isolated in organ baths, precontracted with phenylephrine (0.5 mu m) and relaxant responses were mediated by acetylcholine (0.1-1 mu m), electrical field stimulation (EFS, 1-16 Hz, 0.5 ms, 30 V) or acidified sodium nitrite (a NaNO(2), 0.5 mm). Superoxide anion generators; pyrogallol (50 mu m), hydroquinone (100 mu m), LY 83583 (6-Anilinoquinolin-5,8-quinone, 10 mu m) and superoxide dismutase (SOD) inhibitor; diethyldithiocarbamic acid (DETCA, 8 mm) were used in order to expose corpus cavernosa to oxidant stress. Acetylcholine (0.1-1 mu m) induced relaxant responses were significantly inhibited in LY 83583 (10 mu m) and DETCA + LY 83583 applicated trials. EFS-induced relaxant responses were significantly inhibited in DETCA (8 mm) and DETCA + LY 83583 administrated trials. On the other hand, acidified sodium nitrite-induced responses were inhibited by all of the superoxide anion generators tested. Quercetin (10 mu m) failed to improve the inhibitions on endothelium and electrically stimulated responses. Acidified sodium nitrite (0.5 mm) mediated relaxant responses were significantly restored by quercetin except the groups in which LY 83583 were used. The data suggest that quercetin acts as a protective agent in mouse corpus cavernosum, increasing the bioavailability of exogenous nitric oxide by protecting it from superoxide anion (O(2)-).