Bcl-2 prevents loss of cell viability and caspase activation induced by 3-nitropropionic acid in GT1-7 cells

Ann N Y Acad Sci. 2003 Dec:1010:148-52. doi: 10.1196/annals.1299.024.

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.

MeSH terms

  • Apoptosis / drug effects
  • Apoptosis / physiology*
  • Caspases / metabolism*
  • Cell Line
  • Cell Survival / drug effects*
  • Enzyme Activation / drug effects
  • Humans
  • Hypothalamus / cytology
  • Hypothalamus / physiology
  • Mitochondria / drug effects
  • Mitochondria / physiology
  • Mitochondria / ultrastructure
  • Neurotoxins / toxicity
  • Nitro Compounds
  • Propionates / toxicity*
  • Proto-Oncogene Proteins c-bcl-2 / genetics*

Substances

  • Neurotoxins
  • Nitro Compounds
  • Propionates
  • Proto-Oncogene Proteins c-bcl-2
  • Caspases
  • 3-nitropropionic acid