Plasmid-determined resistance to tetracycline.
A general concept is proposed to explain the mechanism of bacterial resistance to tetracycline, and is essentially based on experimental date and a review of recently of recently published studies. It is assumed that tetracyclines are accumulated in the bacterial cell by an energy-demanding, carrier-mediated influx-mechanism, at a rate depending on the concentration of the antibiotic in the medium. Tetracyclines seep out of the cell by facilitated diffusion at a rate depending on the concentration inside the cell. At steady state, when no net alteration of the intracellular concentration is evident, the molecules of the antibiotic, inside and outside the cell, are exchanged by influx and efflux. In the resistant organism, an additional energy-demanding and carrier-mediated efflux-mechanism is assumed. The total efflux rate is therefore increased, and the steady state is obtained at a lower intracellular level of tetracyclines. It is possible that, in addition, the influx is decreased in the resistant organism.
D001419:Bacteria / Q000187:drug effects* / Q000378:metabolism; D001426:Bacterial Proteins / Q000235:genetics; D001693:Biological Transport, Active; D004058:Diffusion; D005798:Genes, Bacterial; D007700:Kinetics; D011815:R Factors; D013752:Tetracycline / Q000378:metabolism / Q000494:pharmacology*
D001426:Bacterial Proteins; D013752:Tetracycline