Abstract
Cephaloridine produces necrosis of renal proximal tubular cells in humans and experimental animals. The mechanism responsible for this nephrotoxicity still remains unclear. In the present study, cephaloridine toxicity and concomitant changes in tissue glutathione content were determined in rabbits, rats, and mice. Kidney toxicity was evaluated as alterations in kidney-to-body weight ratio, blood urea nitrogen, and kidney slice accumulation of p-aminohippurate and tetraethylammonium. The results demonstrate that cephaloridine is most nephrotoxic to rabbits, intermediate in toxicity to rats, and least toxic to mice, confirming previous histopathological findings. Furthermore, cephaloridine produced a dose-related depletion of glutathione in the renal cortex but not in the medulla shortly after the injection. The relative susceptibility of these three species to glutathione depletion paralleled species differences in nephrotoxicity of cephaloridine. In addition, pretreatment of animals with diethyl maleate potentiated cephaloridine nephrotoxicity, strongly suggesting a relationship between glutathione depletion and cephaloridine toxicity.
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