Calpain-mediated MPP+ toxicity in mitochondrial DNA depleted cells

Neurotox Res. 2008 Jan;13(1):31-8. doi: 10.1007/BF03033365.

Abstract

MPP+ (1-methyl-4-phenylpyridium ion), a complex I - inhibiting metabolite of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), causes anatomic-specific neurodegeneration. To evaluate the broader role of mitochondria in MPP+-induced cell death, we exposed neuron-like NT2 human teratocarcinoma cells with mtDNA rho+ and without mtDNA (rho0) to MPP+. MPP+ minimized the ability of both rho+ and rho0 cells to reduce MTT. Only rho+ cells, though, initiated intrinsic pathway-mediated apoptosis. MPP+ also activated calpains in both rho+ and rho0 cell lines. The calpain inhibitor MDL 28710 was able to prevent the MPP+-related MTT reduction change in rho0 but not rho+ cells. We conclude that 1) MPP+-induced apoptosis requires functional mitochondria, 2) MPP+ activates calpains independent of respiratory chain inhibition, and 3) calpain activation mediates some aspects of MPP+ toxicity.

MeSH terms

  • 1-Methyl-4-phenylpyridinium / toxicity*
  • Apoptosis / drug effects
  • Calpain / metabolism*
  • Caspases / metabolism
  • Cell Line, Tumor
  • DNA, Mitochondrial / metabolism*
  • Electron Transport Complex I / metabolism
  • Humans
  • MPTP Poisoning / genetics
  • MPTP Poisoning / metabolism*
  • MPTP Poisoning / pathology
  • Mitochondria / drug effects
  • Mitochondria / enzymology
  • Nerve Degeneration / genetics
  • Nerve Degeneration / metabolism*
  • Nerve Degeneration / pathology
  • Teratocarcinoma

Substances

  • DNA, Mitochondrial
  • Calpain
  • Caspases
  • Electron Transport Complex I
  • 1-Methyl-4-phenylpyridinium