[Effect of polymyxin B on the conductivity of negatively charged bilayer lipid membranes]. / Vliianie polimiksina B na provodimost' otritsatel'no zarazhennykh bisloinykh lipidnykh membran.

Effect of polymyxin B on the planar bilayer lipid membranes (BLM) formed from synthetic phosphatidic acid has been studied. The addition of cholesterol to phospholipid in molar ratio 1 : 2 was followed by an increase of BLM conductance from 2 x 10(-8) to 3 x 10(-7) Ohm-1 cm-2. It was suggested that the observed increase of conductance was due to the fluidity of the membrane matrix in the presence of cholesterol. It was shown that 10(-6)--10(-5) M polymyxin slightly affected the conductance of BLM from phosphatidic acid. It was found that polymyxin increased conductance of negatively charged BLM modified by palmitic acid from 10(-8) to 10(-6) Ohm-1 cm-2.

[Effect of polymyxin B on ion permeability of bacterial membranes]. / Vliianie polimiksina B na ionnuiu pronitsaemost' bakterial'nykh membran.

Effect of polymyxin B on the movement of K+ and H+ in polymyxin-sensitive cells of E. coli under different metabolic states has been studied. It was shown that polymyxin B induced the efflux of K+, decreased the efflux of H+ and inhibited the consumption of oxygen in bacterial cells. The effect of antibiotic on ion movement was independent of respiratory conditions. It was suggested that polymyxin B increased ion permeability and destroyed lipid-protein interactions of the respiratory chain simultaneously.

[Inhibition of respiration of mitochondria by o-phenanthroline in a constant magnetic field]. / Ingibirovanie dykhaniia mitokhondrii o-fenantrolinom v postoiannom magnitnom pole.

Preincubation of mitochondria treated with chelator of non-heme ferrum o-phenanthroline (0,067-0,267) for 20 min at 18 degrees C in the constant magnetic field of 330 mT brings about a decrease of the intensity of their uncoupled respiration with NAD-dependent substrates by 15-20% as compared to similar mitochondria preparations without the magnetic field effect. The latter is not realized during conjugated respiration with NAD-dependent substrates at uncoupled respiration with succinate, and in the absence of o-phenanthroline as well.

[Effect of polymyxins B and M on oxygen uptake by rat liver mitochondria]. / Deistvie polimiksinov B i M na pogloshchenie kisloroda mitokhondriiami pecheni krys.

Polycationic peptide antibiotics, polymixins B and M, are studied for their effect on oxygen uptake by rat liver mitochondria. They both inhibit the process at state 3 and 3p according to Chance. Low concentrations of polymixin M do not affect oxygen uptake by mitochondria at state 4, but its high concentrations inhibit it. Concentration dependence of polymixin B effect on mitochondria at state 4 is of a bell-like character. Competitive interrelations are found between polymixins M and B in their effect on mitochondria at state 4. Chromatography reveals differences in peptide mobility in a thin layer. It is supposed that polymixin inhibition of oxygen uptake by mitochondria is associated with a disordering effect of the polymixins on the membrane structure during peptide binding to the lipid phase of the membranes. Low concentrations of polymixin B are likely to promote an increase in membrane permeability of mitochondria at state 4.

[Stimulation by quinones of cyanide-resistant respiration in rat liver and heart mitochondria]. / Stimuliatsiia khinonami tsianidrezistentnogo dykhaniia v mitokhondriiakh pecheni i serdtsa krys.

It was shown that hydrophilic benzo- and naphthoquinones stimulate the cyanide-resistant respiration in liver and muscle mitochondria when succinate or NADH and glutamate or malate are used as oxidation substrates. The substrate-dependent oxygen uptake in the presence of cyanide is initiated by menadione, vicasol, 1.2-naphthoquinone, coenzyme Q0 and duroquinone. Rotenone and antimycin A do not inhibit the cyanide-resistant respiration. Oxidation of glutamate and malate in the course of CN-resistant respiration is inhibited by ortho- and bathophenanthroline and p-chloromercurybenzoate, whereas succinate oxidation by tenoyltrifluoroacetone, carboxin and pentachlorophenol. Superoxide dismutase, Cu2+ and catalase inhibit the CN-resistant respiration in the presence of quinones. Addition of catalase to the experimental cell causes O2 release.

[Effect of the polycationic antibiotic polymyxin B on the respiratory activity of rat liver mitochondria]. / Deistvie polikationnogo antibiotika polimiksina v na dykhatel'nuiu aktinvost' mitokhndrii pecheni krys.

the mechanism of the effect of the peptide antibiotic polymixin B on respiration of rat liver mitochondria was studied. It was shown that polymixin B at concentrations of (1,6--2,0) . 10(-3) M inhibits mitochondrial respiration in state 3 and 3u irrespective of the oxidation substrate used and activates oxygen consumption in state 4 at lower concentrations. It is assumed that the antibiotic affects mitochondrial respiration by changing the ionic permeability of the membranes.