Reversible depolarization of in situ mitochondria by oxidative stress parallels a decrease in NAD(P)H level in nerve terminals

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We have reported recently (Chinopoulos et al., 1999 J. Neurochem. 73, 220-228) that mitochondrial membrane potential (ΔΨm) in isolated nerve terminals is markedly reduced by H2O2 in the absence of F0F1-ATPase working as a proton pump. Here we demonstrate that ΔΨm reduced by H2O2 (0.5 mM) in the presence of oligomycin (10 μM), an inhibitor of the F0F1-ATPase, was able to recover by the addition of catalase (2000 U). Similarly, a decrease in the NAD(P)H level due to H2O2 can be reversed by catalase. In addition, H2O2 decreased the ATP level and the [ATP]:[ADP] ratio measured in the presence of oligomycin reflecting an inhibition of glycolysis by H2O2, but this effect was not reversible. The effect of H2O2 on ΔΨm in the presence of the complex I inhibitor, rotenone, was also unaltered by addition of catalase. These results provide circumstantial evidence for a relationship between the decreased NAD(P)H level and the inability of mitochondria to maintain ΔΨm during oxidative stress.

Original languageEnglish
Pages (from-to)483-488
Number of pages6
JournalNeurochemistry international
Issue number6
Publication statusPublished - May 2000



  • ATP
  • Hydrogen peroxide
  • Mitochondrial membrane potential
  • NADH
  • Oligomycin
  • Oxidative stress

ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience
  • Cell Biology

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