Sep 15, 1987

Uncoupling of mitochondrial oxidative phosphorylation by hexetidine

Biochemical and Biophysical Research Communications
G D'ArcangeloE Quagliariello


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 delta psi was also observed. The reported findings show that hexetidine exhibits uncoupling properties.

  • References10
  • Citations8


Mentioned in this Paper

ATP Synthesis Pathway
Resting Potentials
August Rats
Protein Phosphorylation
Carbonyl Cyanide m-Chlorophenyl Hydrazone
Mitochondria, Liver
Acidification - ActCode

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