Hydrogen sulfide: a novel mechanism for the vascular protection by resveratrol under oxidative stress in mouse aorta

Gunay Yetik-Anacak*, Gulnur Sevin, Ozge Ozzayim, Mehmet Vehbi Dereli, Asif Ahmed

*Corresponding author for this work

Research output: Contribution to journalArticle

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.

Original languageEnglish
JournalVascular Pharmacology
VolumeIn press
DOIs
Publication statusPublished - 1 Aug 2016

Fingerprint

Hydrogen Sulfide
Blood Vessels
Aorta
Pyrogallol
Oxidative Stress
Reactive Oxygen Species
Nitric Oxide
Cysteine
resveratrol
Vasodilator Agents
Biological Availability
Antioxidants
Sodium

Bibliographical note

© 2016, Elsevier. Licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International http://creativecommons.org/licenses/by-nc-nd/4.0/

Keywords

  • aorta
  • hydrogen sulfide
  • oxidative stress
  • relaxation
  • resveratrol

Cite this

Yetik-Anacak, Gunay ; Sevin, Gulnur ; Ozzayim, Ozge ; Dereli, Mehmet Vehbi ; Ahmed, Asif. / Hydrogen sulfide : a novel mechanism for the vascular protection by resveratrol under oxidative stress in mouse aorta. In: Vascular Pharmacology. 2016 ; Vol. In press.
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Hydrogen sulfide : a novel mechanism for the vascular protection by resveratrol under oxidative stress in mouse aorta. / Yetik-Anacak, Gunay; Sevin, Gulnur; Ozzayim, Ozge; Dereli, Mehmet Vehbi; Ahmed, Asif.

In: Vascular Pharmacology, Vol. In press, 01.08.2016.

Research output: Contribution to journalArticle

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T2 - a novel mechanism for the vascular protection by resveratrol under oxidative stress in mouse aorta

AU - Yetik-Anacak, Gunay

AU - Sevin, Gulnur

AU - Ozzayim, Ozge

AU - Dereli, Mehmet Vehbi

AU - Ahmed, Asif

N1 - © 2016, Elsevier. Licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International http://creativecommons.org/licenses/by-nc-nd/4.0/

PY - 2016/8/1

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N2 - 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.

AB - 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.

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M3 - Article

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