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Polysulfides (H₂S_n) produced from the interaction of hydrogen sulfide (H₂S) and nitric oxide (NO) activate TRPA1 channels.

ABSTRACT: Hydrogen sulfide (H₂S) exerts synergistic effects with another gaseous signaling molecule nitric oxide (NO) on ion channels and vasculature. However, the mechanism of the synergy is not well understood. Here, we show that the interaction between H₂S and NO generates polysulfides (H₂S_n), which activate transient receptor potential ankyrin 1 (TRPA1) channels. High performance liquid chromatography with tandem mass spectrometry analysis, along with the imaging of intracellular Ca²⁺ and H₂S_n, showed that H₂S_n and their effects were abolished by cyanolysis and by reducing substances such as dithiothreitol (DTT), cysteine, and glutathione (GSH). However, the effects of nitroxyl or nitrosopersulfide, other potential products of H₂S and NO interaction, are not affected by cyanolysis or reducing substances. This study demonstrates that H₂S_n are products of synergy between H₂S and NO and provides a new insight into the signaling mechanisms.

SUBMITTER: Miyamoto R

PROVIDER: S-EPMC5380989 | biostudies-literature | 2017 Apr

REPOSITORIES: biostudies-literature

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Polysulfides (H2Sn) produced from the interaction of hydrogen sulfide (H2S) and nitric oxide (NO) activate TRPA1 channels.

Miyamoto Ryo R Koike Shin S Takano Yoko Y Shibuya Norihiro N Kimura Yuka Y Hanaoka Kenjiro K Urano Yasuteru Y Ogasawara Yuki Y Kimura Hideo H

Scientific reports 20170405

Hydrogen sulfide (H2S) exerts synergistic effects with another gaseous signaling molecule nitric oxide (NO) on ion channels and vasculature. However, the mechanism of the synergy is not well understood. Here, we show that the interaction between H2S and NO generates polysulfides (H2Sn), which activate transient receptor potential ankyrin 1 (TRPA1) channels. High performance liquid chromatography with tandem mass spectrometry analysis, along with the im ...[more]

PMID: 28378773

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Project description:BackgroundSevere acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is involved in a global outbreak affecting millions of people who manifest a variety of symptoms. Coronavirus disease 2019 (COVID-19) caused by SARS-CoV-2 is increasingly associated with cardiovascular complications requiring hospitalizations; however, the mechanisms underlying these complications remain unknown. Nitric oxide (NO) and hydrogen sulfide (H2S) are gasotransmitters that regulate key cardiovascular functions.MethodsBlood samples were obtained from 68 COVID-19 patients and 33 controls and NO and H2S metabolites were assessed. H2S and NO levels were compared between cases and controls in the entire study population and subgroups based on race. The availability of gasotransmitters was examined based on severity and outcome of COVID-19 infection. The performance of H2S and NO levels in predicting COVID-19 infection was also analyzed. Multivariable regression analysis was performed to identify the effects of traditional determinants of gasotransmitters on NO and H2S levels in the patients with COVID-19 infection.ResultsSignificantly reduced NO and H2S levels were observed in both Caucasian and African American COVID-19 patients compared to healthy controls. COVID-19 patients who died had significantly higher NO and H2S levels compared to COVID-19 patients who survived. Receiver-operating characteristic analysis of NO and H2S metabolites in the study population showed free sulfide levels to be highly predictive of COVID-19 infection based on reduced availability. Traditional determinants of gasotransmitters, namely age, race, sex, diabetes, and hypertension had no effect on NO and H2S levels in COVID-19 patients.ConclusionThese observations provide the first insight into the role of NO and H2S in COVID-19 infection, where their low availability may be a result of reduced synthesis secondary to endotheliitis, or increased consumption from scavenging of reactive oxygen species.

Dataset Information

Polysulfides (H₂S_n) produced from the interaction of hydrogen sulfide (H₂S) and nitric oxide (NO) activate TRPA1 channels.

Publications

Polysulfides (H<sub>2</sub>S<sub>n</sub>) produced from the interaction of hydrogen sulfide (H<sub>2</sub>S) and nitric oxide (NO) activate TRPA1 channels.

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