title: Effects of hydrogen sulfide on homocysteine-induced oxidative stress in vascular smooth muscle cells.
abstract: 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.
authors.affiliation: Department of Pathology and Laboratory Medicine, Royal University Hospital, College of Medicine, University of Saskatchewan, 103 Hospital Drive, Saskatoon, Sask., Canada S7N 0W8.
authors.forename: Sheng-Kai
authors.initials: SK
authors.lastname: Yan
authors.forename: Tuanjie
authors.initials: T
authors.lastname: Chang
authors.forename: Hui
authors.initials: H
authors.lastname: Wang
authors.forename: Lingyun
authors.initials: L
authors.lastname: Wu
authors.forename: Rui
authors.initials: R
authors.lastname: Wang
authors.forename: Qing H
authors.initials: QH
authors.lastname: Meng
mesh_terms: D000111:Acetylcysteine / Q000494:pharmacology; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology; D002374:Catalase / Q000378:metabolism; D002460:Cell Line; D005978:Glutathione / Q000494:pharmacology; D006710:Homocysteine / Q000494:pharmacology / Q000502:physiology*; D006862:Hydrogen Sulfide / Q000378:metabolism* / Q000494:pharmacology; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000378:metabolism*; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009861:Onium Compounds / Q000494:pharmacology; D018384:Oxidative Stress; D051381:Rats; D026361:Reactive Nitrogen Species / Q000378:metabolism*; D017382:Reactive Oxygen Species / Q000378:metabolism; D013440:Sulfides / Q000378:metabolism; D013482:Superoxide Dismutase / Q000378:metabolism; D013481:Superoxides / Q000378:metabolism
chemical_list: D000975:Antioxidants; D009861:Onium Compounds; D026361:Reactive Nitrogen Species; D017382:Reactive Oxygen Species; D013440:Sulfides; D006710:Homocysteine; D013481:Superoxides; C007517:diphenyleneiodonium; D002374:Catalase; D013482:Superoxide Dismutase; C025451:sodium bisulfide; D005978:Glutathione; D019331:NG-Nitroarginine Methyl Ester; D000111:Acetylcysteine; D006862:Hydrogen Sulfide