Consumption of H 2 S from Our Daily Diet:
Determination by a Simple Chemosensing Method

Ghosh, Ayndrila; Das, Sujoy; Sarkar, Himadri S.; Kundu, Shampa; Sahoo, Prithidipa

doi:10.1021/acsomega.8b01751

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Consumption of H ₂S from Our Daily Diet: Determination by a Simple Chemosensing Method

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Author(s): Ayndrila Ghosh , Sujoy Das , Himadri S. Sarkar , Shampa Kundu , Prithidipa Sahoo

Publication date (Electronic): 21 September 2018

Journal: ACS Omega

Publisher: American Chemical Society

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Abstract

A unique method has been developed for comparative analysis of H ₂S produced from food samples from our daily diet, both qualitatively and quantitatively. The selective detection of H ₂S has been executed by introducing a simple chemodosimeter ( PN-N ₃) that gives response on the basis of intramolecular charge transfer. UV–vis, fluorimetric, and NMR titrations were performed to demonstrate the sensing mechanism and electronic environment of PN-N ₃ in the presence of H ₂S. Density functional theory calculations were performed to validate the mechanism of azide ( PN-N ₃) reduction to amine ( PN-NH ₂) by the strong reducing power of H ₂S. The potentiality of this chemosensing method is that it could be treated as a simple, less-time-consuming, and cost-effective method for determining H ₂S in biological samples in the nanomolar range.

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Most cited references 55

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H2S as a physiologic vasorelaxant: hypertension in mice with deletion of cystathionine gamma-lyase.

Guangdong Yang, Lingyun Wu, Bo Jiang … (2008)

Studies of nitric oxide over the past two decades have highlighted the fundamental importance of gaseous signaling molecules in biology and medicine. The physiological role of other gases such as carbon monoxide and hydrogen sulfide (H2S) is now receiving increasing attention. Here we show that H2S is physiologically generated by cystathionine gamma-lyase (CSE) and that genetic deletion of this enzyme in mice markedly reduces H2S levels in the serum, heart, aorta, and other tissues. Mutant mice lacking CSE display pronounced hypertension and diminished endothelium-dependent vasorelaxation. CSE is physiologically activated by calcium-calmodulin, which is a mechanism for H2S formation in response to vascular activation. These findings provide direct evidence that H2S is a physiologic vasodilator and regulator of blood pressure.

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Hydrogen sulfide and cell signaling.

Ling Li, Peter Rose, Philip Moore (2011)

Hydrogen sulfide (H₂S) is a gaseous mediator synthesized from cysteine by cystathionine γ lyase (CSE) and other naturally occurring enzymes. Pharmacological experiments using H₂S donors and genetic experiments using CSE knockout mice suggest important roles for this vasodilator gas in the regulation of blood vessel caliber, cardiac response to ischemia/reperfusion injury, and inflammation. That H₂S inhibits cytochrome c oxidase and reduces cell energy production has been known for many decades, but more recently, a number of additional pharmacological targets for this gas have been identified. H₂S activates K(ATP) and transient receptor potential (TRP) channels but usually inhibits big conductance Ca²(+)-sensitive K(+) (BK(Ca)) channels, T-type calcium channels, and M-type calcium channels. H₂S may inhibit or activate NF-κB nuclear translocation while affecting the activity of numerous kinases including p38 mitogen-activated protein kinase (p38 MAPK), extracellular signal-regulated kinase (ERK), and Akt. These disparate effects may be secondary to the well-known reducing activity of H₂S and/or its ability to promote sulfhydration of protein cysteine moieties within the cell.

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Hydrogen sulfide is an endogenous stimulator of angiogenesis.

Andreas Papapetropoulos, Anastasia Pyriochou, Zaid Altaany … (2009)

The goal of the current study was to investigate the role of exogenous and endogenous hydrogen sulfide (H(2)S) on neovascularization and wound healing in vitro and in vivo. Incubation of endothelial cells (ECs) with H(2)S enhanced their angiogenic potential, evidenced by accelerated cell growth, migration, and capillary morphogenesis on Matrigel. Treatment of chicken chorioallantoic membranes (CAMS) with H(2)S increased vascular length. Exposure of ECs to H(2)S resulted in increased phosphorylation of Akt, ERK, and p38. The K(ATP) channel blocker glibenclamide or the p38 inhibitor SB203580 abolished H(2)S-induced EC motility. Since glibenclamide inhibited H(2)S-triggered p38 phosphorylation, we propose that K(ATP) channels lay upstream of p38 in this process. When CAMs were treated with H(2)S biosynthesis inhibitors dl-propylargylglycine or beta-cyano-L-alanine, a reduction in vessel length and branching was observed, indicating that H(2)S serves as an endogenous stimulator of the angiogenic response. Stimulation of ECs with vascular endothelial growth factor (VEGF) increased H(2)S release, while pharmacological inhibition of H(2)S production or K(ATP) channels or silencing of cystathionine gamma-lyase (CSE) attenuated VEGF signaling and migration of ECs. These results implicate endothelial H(2)S synthesis in the pro-angiogenic action of VEGF. Aortic rings isolated from CSE knockout mice exhibited markedly reduced microvessel formation in response to VEGF when compared to wild-type littermates. Finally, in vivo, topical administration of H(2)S enhanced wound healing in a rat model, while wound healing was delayed in CSE(-/-) mice. We conclude that endogenous and exogenous H(2)S stimulates EC-related angiogenic properties through a K(ATP) channel/MAPK pathway.

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Author and article information

Journal

Journal ID (nlm-ta): ACS Omega

Journal ID (iso-abbrev): ACS Omega

Journal ID (publisher-id): ao

Journal ID (coden): acsodf

Title: ACS Omega

Publisher: American Chemical Society

ISSN (Electronic): 2470-1343

Publication date (Electronic): 21 September 2018

Publication date (Print): 30 September 2018

Volume: 3

Issue: 9

Pages: 11617-11623

Affiliations

[1]Department of Chemistry, Visva-Bharati University , Santiniketan 731235, W.B., India

Author notes

[* ]E-mail: prithidipa@ 123456hotmail.com .

Article

DOI: 10.1021/acsomega.8b01751

PMC ID: 6173501

SO-VID: 0017d9bf-8a10-489b-8299-ed18ed05c5ee

License:

This is an open access article published under an ACS AuthorChoice License, which permits copying and redistribution of the article or any adaptations for non-commercial purposes.

History

Date received : 23 July 2018

Date accepted : 10 September 2018

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document-id-old-9 ao8b01751

document-id-new-14 ao-2018-017517

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