title: Bcl-2 prevents loss of cell viability and caspase activation induced by 3-nitropropionic acid in GT1-7 cells.
abstract: In this study, we analyzed the effect of Bcl-2 overexpression, an important anti-apoptotic protein, by using two hypothalamic cell lines, GT1-7puro or GT1-7bcl-2. 3-Nitropropionic acid (3-NP) mediated a dose-dependent decrease in cell viability in GT1-7puro cells, as determined by following the MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) reduction, which was significantly prevented in GT1-7bcl-2 cells. In addition, activation of caspases-2, -3, and -6 induced by 3-NP was prevented by Bcl-2 overexpression. The data suggest that irreversible inhibition of mitochondrial complex II induces apoptotic features of cell death in a process prevented by Bcl-2.
authors.affiliation: Institute of Biochemistry, Faculty of Medicine, and Center for Neuroscience and Cell Biology of Coimbra, University of Coimbra, 3004-504 Coimbra, Portugal.
authors.forename: Olga
authors.initials: O
authors.lastname: Brito
authors.forename: Sandra
authors.initials: S
authors.lastname: Almeida
authors.forename: Catarina R
authors.initials: CR
authors.lastname: Oliveira
authors.forename: A Cristina
authors.initials: AC
authors.lastname: Rego
mesh_terms: D017209:Apoptosis / Q000187:drug effects / Q000502:physiology*; D020169:Caspases / Q000378:metabolism*; D002460:Cell Line; D002470:Cell Survival / Q000187:drug effects*; D004789:Enzyme Activation / Q000187:drug effects; D006801:Humans; D007031:Hypothalamus / Q000166:cytology / Q000502:physiology; D008928:Mitochondria / Q000187:drug effects / Q000502:physiology / Q000648:ultrastructure; D009498:Neurotoxins / Q000633:toxicity; D009574:Nitro Compounds; D011422:Propionates / Q000633:toxicity*; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000235:genetics*
chemical_list: D009498:Neurotoxins; D009574:Nitro Compounds; D011422:Propionates; D019253:Proto-Oncogene Proteins c-bcl-2; D020169:Caspases; C015392:3-nitropropionic acid