title: Hydrogen sulfide: A novel mechanism for the vascular protection by resveratrol under oxidative stress in mouse aorta.
abstract: Reactive oxygen species (ROS) decreases bioavailability of nitric oxide (NO) and impairs NO-dependent relaxations. Like NO, hydrogen sulfide (H2S) is an antioxidant and vasodilator; however, the effect of ROS on H2S-induced relaxations is unknown. Here we investigated whether ROS altered the effect of H2S on vascular tone in mouse aorta and determined whether resveratrol (RVT) protects it via H2S. Pyrogallol induced ROS formation. It also decreased H2S formation and relaxation induced by l-cysteine and in mouse aorta. Pyrogallol did not alter sodium hydrogensulfide (NaHS)-induced relaxation suggesting that the pyrogallol effect on l-cysteine relaxations was due to endogenous H2S formation. RVT inhibited ROS formation, enhanced l-cysteine-induced relaxations and increased H2S level in aortas exposed to pyrogallol suggesting that RVT protects against "H2S-dysfunctions" by inducing H2S formation. Indeed, H2S synthesis inhibitor AOAA inhibited the protective effects of RVT. RVT had no effect on Ach-induced relaxation that is NO dependent and the stimulatory effect of RVT on H2S-dependent relaxation was also independent of NO. These results demonstrate that oxidative stress impairs endogenous H2S-induced relaxations and RVT offers protection by inducing H2S suggesting that targeting endogenous H2S pathway may prevent vascular dysfunctions associated by oxidative stress.
authors.affiliation: Ege University Faculty of Pharmacy Department of Pharmacology, 35100 Bornova-Izmir, Turkey. Electronic address: gunayyetik@gmail.com.
authors.forename: Gunay
authors.initials: G
authors.lastname: Yetik-Anacak
authors.affiliation: Ege University Faculty of Pharmacy Department of Pharmacology, 35100 Bornova-Izmir, Turkey.
authors.forename: Gulnur
authors.initials: G
authors.lastname: Sevin
authors.affiliation: Ege University Faculty of Pharmacy Department of Pharmacology, 35100 Bornova-Izmir, Turkey.
authors.forename: Ozge
authors.initials: O
authors.lastname: Ozzayım
authors.affiliation: Ege University Faculty of Pharmacy Department of Pharmacology, 35100 Bornova-Izmir, Turkey.
authors.forename: Mehmet Vehbi
authors.initials: MV
authors.lastname: Dereli
authors.affiliation: Aston Medical Research Institute, Aston Medical School, Aston University, Aston Triangle, Birmingham B4 7ET, United Kingdom.
authors.forename: Asif
authors.initials: A
authors.lastname: Ahmed
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D001011:Aorta / Q000187:drug effects / Q000378:metabolism; D003545:Cysteine / Q000378:metabolism; D006862:Hydrogen Sulfide / Q000378:metabolism*; D008297:Male; D051379:Mice; D009569:Nitric Oxide / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects*; D011748:Pyrogallol / Q000494:pharmacology; D017382:Reactive Oxygen Species / Q000378:metabolism; D000077185:Resveratrol; D013267:Stilbenes / Q000494:pharmacology*
chemical_list: D000975:Antioxidants; D017382:Reactive Oxygen Species; D013267:Stilbenes; D011748:Pyrogallol; D009569:Nitric Oxide; D003545:Cysteine; D000077185:Resveratrol; D006862:Hydrogen Sulfide
keywords: Aorta; Hydrogen sulfide; Oxidative stress; Relaxation; Resveratrol