NADH regulates the gating of VDAC, the mitochondrial outer membrane channel

M. Zizi, M. Forte, E. Blachly-Dyson, M. Colombini

Research output: Contribution to journalArticlepeer-review

180 Scopus citations


Aerobic energy metabolism in cells involves the transfer of reducing equivalents from organic molecules to oxygen. NADH is important as a carrier of these reducing equivalents and as a feedback regulator of glycolysis. We report that micromolar quantities of NADH double the voltage dependence of the mitochondrial channel, VDAC, a critical pathway for the flux of metabolites between the cytoplasm and the mitochondrial spaces. In the presence of NADH, the opening and closing of this channel is more sensitive to changes in membrane potential and thus presumably better able to respond to changes in metabolic conditions. This effect was observed both on a human and two fungal forms of VDAC, indicating a highly conserved regulatory mechanism. NAD+ and other nucleotides tested failed to mimic the action of NADH. This ability of NADH to facilitate VDAC closure could be one mechanism by which glycolysis can suppress oxidative phosphorylation (Crabtree effect).

Original languageEnglish (US)
Pages (from-to)1614-1616
Number of pages3
JournalJournal of Biological Chemistry
Issue number3
StatePublished - 1994
Externally publishedYes

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology


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