Peyman Ertuğ

Effects of vitamin E and sodium selenate on neurogenic and endothelial relaxation of corpus cavernosum in the diabetic mouse

We studied the effect of vitamin E and sodium selenate treatment on the neurogenic and endothelium-dependent relaxation of isolated corpus cavernosum obtained from streptozotocin-induced diabetic mice. Relaxant responses of corpus cavernosum precontracted by phenylephrine to electrical field stimulation and to acetylcholine were significantly decreased in diabetic mice. There was no significant difference between diabetic and non-diabetic groups for the relaxant response of corpus cavernosum to sodium nitroprusside and papaverine. Treatment with sodium selenate, but not vitamin E, partially prevented the impairment of the neurogenic relaxation, whereas both had a significant, partial restorative action on endothelial dysfunction in corpus cavernosum obtained from diabetic groups. Neither agent exhibited a significant action on the relaxant responses of corpus cavernosum obtained from non-diabetic mice. A decrease in the sensitivity of the neurogenic impairment to antioxidant action may develop more rapidly than that of endothelial dysfunction in streptozotocin-induced diabetic mice.

Comparative study of the quercetin, ascorbic acid, glutathione and superoxide dismutase for nitric oxide protecting effects in mouse gastric fundus

The aim of this work was to compare the preventing capacity of quercetin with Cu/Zn superoxide dismutase (Cu/Zn SOD), ascorbic acid and glutathione on nitric oxide (NO)-induced relaxation in mouse gastric fundus. Furthermore, the effects of the quercetin on the tissue level of total oxidant and antioxidant was investigated. Nitrergic stimulation (4Hz, 25V, 0.1 ms, 10s-train) and exogenous NO (10 μM) induced relaxation. Pyrogallol (10 μM), hydroquinone (100 μM) and LY83583 (6-Anilino-quinolin-5,8-quinone, 5 μM) inhibited nitrergic relaxations. The inhibition observed with pyrogallol, hydroquinone and LY83583 was prevented by quercetin (0.1 μM). Also, ascorbic acid (500 μM), glutathione (100 μM) and Cu/Zn SOD (100 U/ml) prevented the inhibitory effect of superoxide anion generators on the relaxation to nitrergic stimulation and NO. Diethyldithiocarbamic acid (DETCA; 8mM) inhibited nitrergic relaxations. DETCA-induced inhibition on nitrergic stimulation and NO-induced relaxation was prevented by quercetin, ascorbic acid, glutathione or Cu/Zn SOD. DETCA plus pyrogallol, hydroquinone or LY83583 strengthened the inhibition on the relaxations. Also, pre-treatment with quercetin, ascorbic acid and glutathione prevented the inhibitory effect of DETCA plus LY-83583 on the relaxation to nitrergic stimulation and NO but Cu/Zn SOD did not prevent this inhibition. Also, quercetin increased tissue total antioxidant capacity and decreased tissue oxidant level and oxidative stress index in DETCA-treatment group. These results indicate that quercetin has antioxidant effect and protects NO from endogenous superoxide anion-driven inactivation and enhances its biological activity, suggesting that quercetin may scavenge superoxide anion in a Cu/Zn SOD, glutathione or ascorbic acid-inhibitable manner.

Protective effect of quercetin, a polyphenolic compound, on mouse corpus cavernosum.

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 μm) and relaxant responses were mediated by acetylcholine (0.1–1 μm), electrical field stimulation (EFS, 1–16 Hz, 0.5 ms, 30 V) or acidified sodium nitrite (a NaNO2, 0.5 mm). Superoxide anion generators; pyrogallol (50 μm), hydroquinone (100 μm), LY 83583 (6‐Anilinoquinolin‐5,8‐quinone, 10 μm) 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 μm) induced relaxant responses were significantly inhibited in LY 83583 (10 μm) 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 μm) 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 (O2–).

Ethanol-induced relaxation of mouse esophagus: subcellular mechanisms

Ethanol (164 mm) produced reproducible relaxations in isolated mouse esophageal strips. Hexamethonium (10–500 μm), a ganglionic blocking agent, and lidocaine (10–100 μm), a local anesthetic agent, failed to affect the relaxations induced by ethanol in the mouse esophagus. Although verapamil (10–500 μm), a selective blocker of L‐type Ca2+ channels, failed to affect the relaxations to ethanol, ruthenium red (10–100 μm), a selective blocker of ryanodine receptors (intracellular Ca2+ channels), and cyclopiazonic acid (1–10 μm), a selective blocker of sarcoplasmic reticulum Ca2+ ATPase (SERCA), significantly inhibited these relaxations. In addition, tetraethylammonium (10–100 μm), a potassium‐selective ion channel blocker and Nω‐nitro‐l‐arginine (l‐NOARG; 10–500 μm), a specific inhibitor of nitric oxide synthase (NOS), neomycin (10–500 μm), a phospholipase C inhibitor and indomethacine (1–10 μm), a non‐selective COX inhibitor, significantly inhibited the relaxations induced by ethanol. In contrast ouabain (10–100 μm), 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 Ca2+ 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.

Prejunctional facilitatory effect of a thiol‐alkylating agent N‐Ethylmaleimide on neurogenic contractions in rat prostate smooth muscle

The effect of a non‐specific thiol‐alkylating agent N‐ethylmaleimide (NEM) was studied on neurogenic contractile mechanisms in rat ventral prostate gland.