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The Antioxidant Properties of Glucosinolates in Cardiac Cells Are Independent of H 2 S Signaling.

Authors :
Harvey, Félix
Aromokunola, Boluwaji
Montaut, Sabine
Yang, Guangdong
Source :
International Journal of Molecular Sciences; Jan2024, Vol. 25 Issue 2, p696, 14p
Publication Year :
2024

Abstract

The organic sulfur-containing compounds glucosinolates (GSLs) and the novel gasotransmitter H<subscript>2</subscript>S are known to have cardioprotective effects. This study investigated the antioxidant effects and H<subscript>2</subscript>S-releasing potential of three GSLs ((3E)-4-(methylsulfanyl)but-3-enyl GSL or glucoraphasatin, 4-hydroxybenzyl GSL or glucosinalbin, and (R<subscript>S</subscript>)-6-(methylsulfinyl)hexyl GSL or glucohesperin) in rat cardiac cells. It was found that all three GSLs had no effect on cardiac cell viability but were able to protect against H<subscript>2</subscript>O<subscript>2</subscript>-induced oxidative stress and cell death. NaHS, a H<subscript>2</subscript>S donor, also protected the cells from H<subscript>2</subscript>O<subscript>2</subscript>-stimulated oxidative stress and cell death. The GSLs alone or mixed with cysteine, N-acetylcysteine, glutathione, H<subscript>2</subscript>O<subscript>2</subscript>, iron and pyridoxal-5′-phosphate, or mouse liver lysates did not induce H<subscript>2</subscript>S release. The addition of GSLs also did not alter endogenous H<subscript>2</subscript>S levels in cardiac cells. H<subscript>2</subscript>O<subscript>2</subscript> significantly induced cysteine oxidation in the cystathionine gamma-lyase (CSE) protein and inhibited the H<subscript>2</subscript>S production rate. In conclusion, this study found that the three tested GSLs protect cardiomyocytes from oxidative stress and cell death but independently of H<subscript>2</subscript>S signaling. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
16616596
Volume :
25
Issue :
2
Database :
Complementary Index
Journal :
International Journal of Molecular Sciences
Publication Type :
Academic Journal
Accession number :
175075063
Full Text :
https://doi.org/10.3390/ijms25020696