Uncoupling of mitochondrial oxidative phosphorylation by hexetidine

Gabriella D'Arcangelo, Maria Barile, Salvatore Passarella, Ernesto Quagliariello

Research output: Contribution to journalArticlepeer-review

2 Scopus citations


To gain further insight into the biochemical properties of the antibacterial hexetidine, isolated rat liver mitochondria were added with this drug and investigation made of certain features related to mitochondrial bioenergetics. Hexetidine was found to cause oxidation of intramitochondrial pyridine nucleotides and stimulate the rate of oxygen uptake caused by respiratory substrates involving three, two and one site(s) of phosphorylation. Reversal of oxygen uptake inhibition by oligomycin was also determined. By investigating hexetidine effect on oxidative phosphorylation, hexetidine was found both to inhibit the rate of ATP synthesis and to cause ATP hydrolysis. Likewise, hexetidine capability to produce acidification of extramitochondrial medium and to collapse ΔΨ was also observed. The reported findings show that hexetidine exhibits uncoupling properties.

Original languageEnglish (US)
Pages (from-to)801-808
Number of pages8
JournalBiochemical and Biophysical Research Communications
Issue number2
StatePublished - Sep 15 1987

All Science Journal Classification (ASJC) codes

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology


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