Effects of hydrogen sulfide on homocysteine-induced oxidative stress in vascular smooth muscle cells

被引:175
作者
Yan, Sheng-Kai
Chang, Tuanjie
Wang, Hui
Wu, Lingyun
Wang, Rui [1 ]
Meng, Qing H.
机构
[1] Lakehead Univ, Dept Biol, Thunder Bay, ON P7B 5E1, Canada
[2] Univ Saskatchewan, Royal Univ Hosp, Coll Med, Dept Pathol & Lab Med, Saskatoon, SK S7N 0W8, Canada
[3] Univ Saskatchewan, Coll Med, Dept Pharmacol, Saskatoon, SK S7N 5E5, Canada
基金
加拿大健康研究院;
关键词
hydrogen sulfide; homocysteine; reactive oxygen species; vascular smooth muscle cells;
D O I
10.1016/j.bbrc.2006.10.058
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Hydrogen sulfide (H2S) 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 H2S 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 H2S). HCY induced cytotoxicity, increased levels of H2O2, ONOO-, and O-2(center dot-) in a time- and concentration-dependent manner. Low levels of NaHS (30 or 50 mu M) protected A-10 cells from cytotoxicity, decreased the production of H2O2, ONOO-, and O-2(center dot-) 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(center dot-) formation induced by HCY. In conclusion, our findings provide the first evidence that low levels of H2S decrease reactive oxygen species and improve cell viability and by doing so limit cellular damage induced by HCY. (c) 2006 Elsevier Inc. All rights reserved.
引用
收藏
页码:485 / 491
页数:7
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