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Mechanisms of gentamicin-induced dysfunction of renal cortical mitochondria: II. Effects on mitochondrial monovalent cation transport
Authors:Joel M. Weinberg  Phillip G. Harding  H.David Humes
Affiliation:Division of Nephrology, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan 48109 U.S.A.
Abstract:Mitochondrial swelling techniques were used to evaluate the effects of the aminoglycoside antibiotic gentamicin on renal cortical mitochondrial monovalent cation permeability. Gentamicin behaved like EDTA to enhance energy-dependent Na+- and K+-acetate uptake with a relatively greater effect on Na+-acetate uptake. Mg2+ prevented and reversed the effects of both EDTA and gentamicin. Neither agent affected energy-independent uptake of Na+ and K+-acetate. Gentamicin did not enhance energy-independent uptake of K+- and Na+-nitrate. Gentamicin enhanced energy-dependent swelling in a chloride- and phosphate-containing medium as a function of the medium Na+ and K+ concentration. This effect occurred simultaneously with gentamicin-induced stimulation of State 4 respiration and was blocked by Mg2+. Gentamicin did not affect phosphate transport. The results are taken to indicate a specific action of gentamicin to enhance mitochondrial monovalent cation permeability at an Mg2+-sensitive site and it is proposed that this accounts for the effects of gentamicin on mitochondrial respiration.
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