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[Effect of polymyxins B and M on oxygen uptake by rat liver mitochondria]

Ukrainskii Biokhimicheskii Zhurnal (1978)
|March 1, 1984
PubMed

Insights

Polymyxins B and M antibiotics inhibit mitochondrial respiration. Polymyxins disrupt mitochondrial membranes, affecting oxygen uptake, with Polymyxin B potentially increasing membrane permeability at low doses.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Pharmacology

Background:

  • Polycationic peptide antibiotics, polymixins B and M, are crucial in treating multidrug-resistant Gram-negative bacterial infections.
  • Mitochondria are vital cellular organelles responsible for energy production through oxidative phosphorylation.

Purpose of the Study:

  • To investigate the effects of polymixins B and M on the oxygen uptake of rat liver mitochondria.
  • To elucidate the mechanism underlying polymixin-induced inhibition of mitochondrial respiration.

Main Methods:

  • Measurement of mitochondrial oxygen consumption rates at different respiratory states (state 3, 3p, and 4) using a Clark-type oxygen electrode.
  • Thin-layer chromatography was employed to analyze the mobility and potential differences between polymyxins B and M.
  • Assessment of competitive interactions between polymixins B and M.

Main Results:

  • Both polymyxins B and M significantly inhibited mitochondrial respiration at state 3 and 3p.
  • Polymixin M inhibited state 4 respiration only at high concentrations, whereas polymixin B exhibited a bell-shaped concentration-dependent effect on state 4 respiration.
  • Competitive interrelations were observed between polymixins B and M concerning their effects on state 4 respiration.
  • Chromatographic analysis revealed distinct mobilities for polymyxins B and M.

Conclusions:

  • Polymyxin inhibition of mitochondrial oxygen uptake is likely due to membrane structure disordering upon peptide binding to the lipid phase.
  • Low concentrations of polymyxin B may enhance mitochondrial membrane permeability at state 4.
  • Polymyxins B and M exhibit differential effects on mitochondrial respiration, suggesting distinct interaction mechanisms with the mitochondrial membrane.

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