The renal toxicity of (R)-3-chlorolactate in the rat |
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| Authors: | K E Porter A R Jones |
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| Affiliation: | 1. Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, P.O. Box 22452, Riyadh 11459, Saudi Arabia;2. Pharm D program, College of Pharmacy, King Saud University, P.O. Box 22452, Riyadh 11459, Saudi Arabia;3. Statistics Deanship of Scientific Research, College of Humanities and Social Sciences, King Saud University, P.O. Box 2456, Riyadh 11451, Saudi Arabia;1. Departamento de Ciências Patológicas, Centro de Ciências Biológicas, Universidade Estadual de Londrina, 86057-970 Londrina, Paraná, Brazil;2. Laboratório de Anatomia Patológica, Centro de Ciências de Saúde, Universidade Estadual de Londrina, 86038-350 Londrina, Paraná, Brazil;3. Departamento de Ciências Farmacêuticas, Centro de Ciências da Saúde, Universidade Estadual de Londrina, 86038-350 Londrina, Paraná, Brazil |
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| Abstract: | ![]()
The renal toxicity of (R,S)-3-chlorolactate has been shown to be due to the (R)-isomer which, when administered to rats, induces diuresis and glucosuria. The metabolic activity of isolated tubule cells, prepared from rat kidney, was inhibited by (R)-3-chlorolactate and the action of the compound was localised as affecting mitochondrial metabolism. Studies with kidney mitochondria pin-pointed the site of action as being involved with the oxidative metabolism of malate but not the inhibition of mitochondrial malate dehydrogenase. The effects of oxalate, a metabolite of (R)-3-chlorolactate, and of (R,S)-3-chlorolactaldehyde on renal tubule cells was investigated. While some degrees of inhibition of metabolic activity were evident, these compounds were not responsible for the toxic effects produced by (R)-3-chlorolactate. |
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