Mechanism of renal distribution of aminoglycoside antibotics.
The renal accumulation of dibekacin, one of the aminoglycoside antibiotics, was pharmacokinetically analyzed and the mechanism of the renal accumulation of these antibiotics was investigated. The remaining amounts of dibekacin in the kidneys were adequately expressed by the bi-exponential equation. There was no possibility of a covalent bond between dibekacin and the renal tissue components. The renal accumulation of the aminoglycoside antibiotics was explained in terms of the two successive processes, renal tubular reabsorption and electrostatic interaction between these antibiotics and the tissue components. In other words, these antibiotics were reabsorbed at the renal tubules and transported into renal tubular epithelial cells and bound to the tissue components by electrostatic force. The electrostatic interaction also played an important role in increasing the acute toxicities of aminoglycoside antibiotics.
D000617:Aminoglycosides / Q000378:metabolism; D000818:Animals; D000900:Anti-Bacterial Agents / Q000378:metabolism*; D006493:Heparin / Q000378:metabolism; D007668:Kidney / Q000378:metabolism*; D008297:Male; D051381:Rats; D014018:Tissue Distribution
D000617:Aminoglycosides; D000900:Anti-Bacterial Agents; D006493:Heparin