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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 microm) and relaxant responses were mediated by acetylcholine (0.1-1 microm), 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 microm), hydroquinone (100 microm), LY 83583 (6-Anilinoquinolin-5,8-quinone, 10 microm) 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 microm) induced relaxant responses were significantly inhibited in LY 83583 (10 microm) 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 microm) 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)(-)).

Ethanol (164 mm) produced reproducible relaxations in isolated mouse esophageal strips. Hexamethonium (10-500 microm), a ganglionic blocking agent, and lidocaine (10-100 microm), a local anesthetic agent, failed to affect the relaxations induced by ethanol in the mouse esophagus. Although verapamil (10-500 microm), a selective blocker of L-type Ca(2+) channels, failed to affect the relaxations to ethanol, ruthenium red (10-100 microm), a selective blocker of ryanodine receptors (intracellular Ca(2+) channels), and cyclopiazonic acid (1-10 microm), a selective blocker of sarcoplasmic reticulum Ca(2+) ATPase (SERCA), significantly inhibited these relaxations. In addition, tetraethylammonium (10-100 microm), a potassium-selective ion channel blocker and N(omega)-nitro-l-arginine (l-NOARG; 10-500 microm), a specific inhibitor of nitric oxide synthase (NOS), neomycin (10-500 microm), a phospholipase C inhibitor and indomethacine (1-10 microm), a non-selective COX inhibitor, significantly inhibited the relaxations induced by ethanol. In contrast ouabain (10-100 microm), an inhibitor of Na(+)-K(+)-ATPase, failed to cause significant alteration on these relaxations in the same tissue. The results of the present study suggest that the inhibitory effect of ethanol on the mouse esophagus may be direct effect of ethanol on the muscle tissue rather than neuronal effect. In addition, intracellular but not extracellular Ca(2+) may have a role on ethanol-induced relaxations in isolated mouse esophageal strips. Potassium channels and nitric oxide may also have a role on these relaxations. Similarly, phospholypase C and arachidonic acid pathways may contribute the relaxations to ethanol. However Na(+)-K(+)-ATPase may not have a role on relaxations induced by ethanol in the mouse esophagus.