Abstract
Hydrogen sulfide (H 2S) is an important gasotransmitter that generated in mammalian cells from l-cysteine metabolism. Little is known about its protective role in oxidative stress. In the present study, we investigated whether H 2S could affect homocysteine (HCY)-induced cytotoxicity and oxidative stress in vascular smooth muscle cells. Cultured A-10 cells were exposed to HCY treatment in the presence or absence of NaHS (donor of H 2S). HCY induced cytotoxicity, increased levels of H 2O 2, ONOO −, and O 2 - in a time- and concentration-dependent manner. Low levels of NaHS (30 or 50 μM) protected A-10 cells from cytotoxicity, decreased the production of H 2O 2, ONOO −, and O 2 - in the presence of HCY. Furthermore, NaHS enhanced inhibitory effects of NAC, GSH, DPI, SOD, L-NAME, or vitamin C on oxidized DCF or O 2 - formation induced by HCY. In conclusion, our findings provide the first evidence that low levels of H 2S decrease reactive oxygen species and improve cell viability and by doing so limit cellular damage induced by HCY.
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More From: Biochemical and Biophysical Research Communications
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