Study summary · research use only
Protonophoric action of BAM15 on planar bilayers, liposomes, mitochondria, bacteria and neurons
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
This study examined the protonophoric mechanism of BAM15 ((2-fluorophenyl){6-[(2-fluorophenyl)amino](1,2,5-oxadiazolo[3,4-e]pyrazin-5-yl)}amine) using planar bilayer lipid membranes, liposomes, isolated rat liver mitochondria, the bacterium Bacillus subtilis, and molluscan neurons, compared with the classical protonophoric uncoupler CCCP. The abstract reports that BAM15 acted as an anionic protonophore in planar membranes and liposomes with potency close to CCCP, caused membrane potential collapse, increased respiration rate, and induced Ca2+ efflux in rat liver mitochondria at concentrations slightly higher than CCCP, and that its uncoupling action, unlike CCCP's, was partially reversed by the adenine nucleotide translocase inhibitor carboxyatractyloside. It also inhibited growth of Bacillus subtilis at micromolar concentrations and altered electrical activity in molluscan neurons more slowly than CCCP.
Abstract
Small molecules capable of uncoupling respiration and ATP synthesis in mitochondria are protective towards various cell malfunctions. Recently (2-fluorophenyl){6-[(2-fluorophenyl)amino](1,2,5-oxadiazolo[3,4-e]pyrazin-5-yl)}amine (BAM15), a new compound of this type, has become popular as a potent mitochondria-selective depolarizing agent producing minimal adverse effects. To validate protonophoric mechanism of BAM15 action, we examined its behavior in bilayer lipid membranes (BLM). BAM15 proved to be a typical anionic protonophore with the activity on planar membranes being suppressed upon decreasing membrane dipole potential. In both planar BLM and liposomes, BAM15 induced proton conductance with the potency close to that of the classical protonophoric uncoupler carbonyl cyanide m-chlorophenyl hydrazone (CCCP). In isolated rat liver mitochondria (RLM), BAM15 caused membrane potential collapse, increased respiration rate and induced Ca2+ efflux at concentrations slightly higher than those for CCCP. Surprisingly, the uncoupling action of BAM15 on isolated RLM, in contrast to that of CCCP, was partially reversed by carboxyatractyloside (CATR), an inhibitor of adenine nucleotide translocase, thereby indicating involvement of this protein in the BAM15-induced uncoupling. BAM15 inhibited growth of Bacillus subtilis at micromolar concentrations. In electrophysiological experiments on molluscan neurons, BAM15 caused plasma membrane depolarization and suppression of electrical activity, but the effect developed more slowly than that of CCCP.
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