Gentamicin is a bactericidal aminoglycoside antibiotic and an important agent for the treatment of many serious gram-negative bacillary infections. However, emergence of resistant microorganisms and development of nephrotoxicity with long-term use of the antibiotic has become a serious problem and may limit the future use of this agent.
It is generally accepted that gentamicin-induced nephrotoxicity is closely related to the accumulation of the antibiotic in renal tubules.
This study was made to determine the changes in the activities of alk~dine phosphatase and adenosine triphosphatase (ATPase) histochemically in renal tubules of male ICR mice, weighing 20-25 gm, treated with a bolus intraperitoneal injection of gentamicin, 300 mg per kg body weight at 3, 6 and 12 hours after drug administration in order to elucidate the pathogenesis underlying gentamicin-induced nephrotoxicity.
The results were as follows.
1. Phosphatase activities after gentamicin administration were decreased in renal cortex.
2. Alkaline phosphatase activity in renal cortex were slightly decreased (´++) at 3 and 12 hours and moderately decreased (+) at 6 hours after drug administration compared to control group (1E+).
3. ATPase activity in renal cortex were moderately decreased (+) at 3 hours, severe decreased () at 6 hours and slightly decreased (4) at 12 hours after drug administration compared to control group 00.
Consequently, it is suggested that gentamicin decreases in activities of alkaline phosphatase and ATPase in the kidney by damages in renal epithelial cells and cytoplasmic organelles and thought to be that it is one of the biochemical events in gentamicin-induced nephrotoxicity.
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