Yan Sheng-Kai, Chang Tuanjie, Wang Hui, Wu Lingyun, Wang Rui, Meng Qing H
Department of Pathology and Laboratory Medicine, Royal University Hospital, College of Medicine, University of Saskatchewan, 103 Hospital Drive, Saskatoon, Sask., Canada S7N 0W8.
Biochem Biophys Res Commun. 2006 Dec 15;351(2):485-91. doi: 10.1016/j.bbrc.2006.10.058. Epub 2006 Oct 18.
Hydrogen sulfide (H(2)S) 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(2)S 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(2)S). HCY induced cytotoxicity, increased levels of H(2)O(2), ONOO(-), and O2- in a time- and concentration-dependent manner. Low levels of NaHS (30 or 50microM) protected A-10 cells from cytotoxicity, decreased the production of H(2)O(2), ONOO(-), and O2- in the presence of HCY. Furthermore, NaHS enhanced inhibitory effects of NAC, GSH, DPI, SOD, L-NAME, or vitamin C on oxidized DCF or O2- formation induced by HCY. In conclusion, our findings provide the first evidence that low levels of H(2)S decrease reactive oxygen species and improve cell viability and by doing so limit cellular damage induced by HCY.
硫化氢（H₂S）是一种重要的气体信号分子，由哺乳动物细胞中L-半胱氨酸代谢产生。关于其在氧化应激中的保护作用知之甚少。在本研究中，我们调查了H₂S是否会影响同型半胱氨酸（HCY）诱导的血管平滑肌细胞的细胞毒性和氧化应激。将培养的A-10细胞在有或无NaHS（H₂S供体）的情况下进行HCY处理。HCY以时间和浓度依赖性方式诱导细胞毒性，增加H₂O₂、ONOO⁻和O₂⁻的水平。低水平的NaHS（30或50μM）可保护A-10细胞免受细胞毒性，在存在HCY的情况下降低H₂O₂、ONOO⁻和O₂⁻的产生。此外，NaHS增强了NAC、GSH、DPI、SOD、L-NAME或维生素C对HCY诱导的氧化DCF或O₂⁻形成的抑制作用。总之，我们的研究结果提供了首个证据，即低水平的H₂S可减少活性氧并提高细胞活力，从而限制HCY诱导的细胞损伤。
