Effect of rifampicin derivatives on the ion compartmentation of biological membranes.
Based on the experimental results that 3-formyl rifamycin SV acts as an uncoupler in vitro on rat liver mitochondria, the effect of some rifampicin derivatives on the K+ and H+ compartmentation of biological membranes was examined to obtain a chemiosmotic hypothesis for oxidative phosphorylation. The K+ release from mitochondria was remarkably stimulated by 3-formyl rifamycin SV in accordance with uncoupling of the oxidative phosphorylation. 3-Formyl rifamycin SV also stimulated the K+ release from red blood cells, though its action was not as effective as in mitochondria. It can be suggested that 3-formyl rifamycin SV interacts with biological membranes, causing a change in permeability to ions, especially of K+ and H+ through the mitochondrial membrane, resulting in uncoupling of the oxidative phosphorylation.
D000818:Animals; D004910:Erythrocyte Membrane / Q000187:drug effects* / Q000378:metabolism; D004912:Erythrocytes / Q000187:drug effects*; D006859:Hydrogen / Q000378:metabolism; D066298:In Vitro Techniques; D008297:Male; D008566:Membranes / Q000187:drug effects / Q000378:metabolism; D008930:Mitochondria, Liver / Q000187:drug effects / Q000378:metabolism / Q000648:ultrastructure*; D010101:Oxygen Consumption / Q000187:drug effects; D011188:Potassium / Q000378:metabolism*; D011506:Proteins / Q000378:metabolism; D011817:Rabbits; D051381:Rats; D012293:Rifampin / Q000031:analogs & derivatives* / Q000494:pharmacology; D013997:Time Factors
D011506:Proteins; D006859:Hydrogen; D011188:Potassium; D012293:Rifampin