title: Reactive oxygen species from mitochondria mediate SW480 cells apoptosis induced by Na2SeO3.
abstract: A number of selenium compounds have been found to inhibit tumorigenesis in a variety of animal and cell models. In order to explore the molecular mechanism involved in the anticarcinogenesis activity of selenium, we examined the effects of sodium selenite on cell viabilty, generation of reactive oxygen species (ROS), and mitochondrial transmembrane potential (delta(psi)m) in human colonic carcinoma cells SW480. The result from MTT test showed that sodium selenite reduced cell viability. Morophologic and flow cytometric results indicated that Na2SeO3 induced the apoptosis of SW480 cells. Na2SeO3 increased the generation of intracellular ROS, whereas BAPTA-AM, rotenone, and NaCN completely inhibited the increase of ROS induced by Na2SeO3. Na2SeO3 also caused the disruption of delta(psi)m. The intracellular ROS increase and apoptosis induced by Na2SeO3 were significantly decreased by superoxide dismutase (SOD), catalase. These data suggest that the ROS mediate apoptosis induced by Na2SeO3 and mitochondria may be a major source of Na2SeO3-induced ROS.
authors.affiliation: Department of Chemistry, Huazhong University of Science and Technology, Wuhan, People's Republic of China.
authors.forename: Hai-Tao
authors.initials: HT
authors.lastname: Wang
authors.forename: Xiang-Liang
authors.initials: XL
authors.lastname: Yang
authors.forename: Zhi-Hong
authors.initials: ZH
authors.lastname: Zhang
authors.forename: Jing-Ling
authors.initials: JL
authors.lastname: Lu
authors.forename: Hui-Bi
authors.initials: HB
authors.lastname: Xu
mesh_terms: D017209:Apoptosis / Q000187:drug effects*; D002374:Catalase / Q000378:metabolism / Q000494:pharmacology; D002455:Cell Division / Q000187:drug effects; D048429:Cell Size / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects; D002614:Chelating Agents / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D004533:Egtazic Acid / Q000031:analogs & derivatives* / Q000494:pharmacology; D005434:Flow Cytometry; D006801:Humans; D007425:Intracellular Membranes / Q000187:drug effects / Q000378:metabolism; D008564:Membrane Potentials / Q000187:drug effects; D008928:Mitochondria / Q000378:metabolism*; D017382:Reactive Oxygen Species / Q000378:metabolism*; D012402:Rotenone / Q000494:pharmacology; D012966:Sodium Cyanide / Q000494:pharmacology; D018038:Sodium Selenite / Q000494:pharmacology*; D013482:Superoxide Dismutase / Q000378:metabolism / Q000494:pharmacology; D013997:Time Factors; D014407:Tumor Cells, Cultured
chemical_list: D002614:Chelating Agents; D017382:Reactive Oxygen Species; D012402:Rotenone; D004533:Egtazic Acid; D002374:Catalase; D013482:Superoxide Dismutase; D018038:Sodium Selenite; C025603:1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid; D012966:Sodium Cyanide