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 (HS) is an antioxidant and vasodilator; however, the effect of ROS on HS-induced relaxations is unknown. Here we investigated whether ROS altered the effect of HS on vascular tone in mouse aorta and determined whether resveratrol (RVT) protects it via HS. Pyrogallol induced ROS formation. It also decreased HS 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 HS formation. RVT inhibited ROS formation, enhanced l-cysteine-induced relaxations and increased HS level in aortas exposed to pyrogallol suggesting that RVT protects against "HS-dysfunctions" by inducing HS formation. Indeed, HS 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 HS-dependent relaxation was also independent of NO. These results demonstrate that oxidative stress impairs endogenous HS-induced relaxations and RVT offers protection by inducing HS suggesting that targeting endogenous HS pathway may prevent vascular dysfunctions associated by oxidative stress.

Do penile haemodynamics change in the presence of hydrogen sulphide (H2S) donor in metabolic syndrome-induced erectile dysfunction?

“…Although the glucose level was not significantly higher, the decreased H 2 S formation in metS group in our study suggest that the role of metabolic factors was responsible for impairment of H 2 S level rather than hyperglycaemia, as endogenous H 2 S production was significantly decreased in penile tissues or corpus cavernosum smooth muscle cell culture under hyperglycaemic conditions (Zhang et al., ). This decrease also may be due to oxidative stress, as it has previously been shown that oxidative stress leads to decrease in both basal and L‐cysteine‐stimulated H 2 S formation in aorta (Yetik‐Anacak et al., ), and it is very well known that oxidative stress plays an important role in metS and ED (Jeremy et al., ). However, we should note that although we did not measure 3‐mercaptypyruvate sulphurtransferase (MPST)‐induced H 2 S formation specifically, it is possible that H 2 S formation through this enzyme may also be impaired, as a decrease in MPST‐dependent H 2 S formation was shown in hyperglycaemia (Coletta et al., ).…”

“…showed compensatory and increased significant role of H 2 S to maintain vasorelaxation in penis in eNOS deficiency (Yetik‐Anacak et al., ). The beneficial effect of H 2 S donors on metS‐induced ED may include not only their vasodilator effects in penis but also PDE inhibition (Bucci et al., ), antioxidant (Yetik‐Anacak et al., ) and angiogenic effects as well (Papapetropoulos et al., ).…”

“…All samples were assayed in duplicate, and H 2 S concentration was calculated against a calibration curve of NaHS (3.9–250 μ m ). Data were calculated as nanomoles per milligram of protein.min −1 (Yetik‐Anacak, Sevin, Ozzayim, Dereli, & Ahmed, ; Yetik‐Anacak et al., ).…”

Bisphenol A vascular toxicity: Protective effect of Vitis vinifera (grape) seed extract and resveratrol

“…Chronic exposure to resveratrol (50 mg/l in drinking water for 21 days) increased the production of NO and nitrite/nitrate level and decreased superoxide production in the rat aorta (Soylemez, Gurdal, Sepici, & Akar, ). Furthermore, Yetik‐Anacak, Sevin, Ozzayım, Dereli, and Ahmed () proposed vaso‐protective effects of resveratrol against oxidative stress via inducing H 2 S pathway in mouse aorta (Yetik‐Anacak et al, ).…”

Potential role of hydrogen sulfide in diabetes-impaired angiogenesis and ischemic tissue repair

“…Several lines of evidence indicate that H 2 S has a role in the regulation of vascular tone. H 2 S induced vascular relaxation in aorta [ [78] , [79] , [80] ], gastric artery [ 81 ], mesenteric artery [ 5 , 82 ], and internal mammary artery [ 83 ]. Accumulative evidence indicate that H 2 S is an EDHF [ 5 , [17] , [18] , [19] , [20] , 82 , [84] , [85] , [86] ].…”