MITOCHONDRIAL DYSFUNCTION AT THE EARLY STAGE OF CISPLATIN-INDUCED ACUTE RENAL FAILURE IN RATS

来源 :Journal of Zhejiang University Science | 被引量 : 0次 | 上传用户:qq503302228
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The present study was undertaken to clarify the pathogenesis of cisplatin induced acute renal failure at the early stage. Male Sprague Dawley rats were given an intravenous administration of 10 mg/kg cisplatin. 0.9% saline was infused into them at a rate of 2 ml/h for 3 h, starting with a 2 ml bolus injection before cisplatin administration. 3 h following cisplatin administration, no evident morphological abnormalities were found by both light and electron microscopy; there were also no significant changes in GFR. Thirty min after cisplatin injection, urine sodium and potassium excretion increased by 56% and 260% those of the control animals, respectively. Apparent renal mitochondrial respiration dysfunction was observed in cisplatin treated rats 3 h later; the state 4 respiration increased by 100% and state 3 respiration, respiratory control ratio and carbonyl cyanide p trifluoromethoxyphenyl hydrazone uncoupled respiration decreased by 46%, 74% and 47% of the controls, respectively. The present data suggest that mitochondrial dysfunction may be a very early event in cisplatin induced acute renal failure in rats. The present study was undertaken to clarify the pathogenesis of cisplatin induced acute renal failure at the early stage. Male Sprague Dawley rats were given an intravenous administration of 10 mg / kg cisplatin. 0.9% saline was infused into them at a rate of 2 ml / h for 3 h, starting with a 2 ml bolus injection before cisplatin administration. 3 h following cisplatin administration, no evident morphological abnormalities were found by both light and electron microscopy; there were also no significant changes in GFR. Thirty min after cisplatin administration, urine sodium and potassium excretion increased by 56% and 260% those of the control animals, respectively. Apparent renal mitochondrial respiration dysfunction was observed in cisplatin treated rats 3 h later; the state 4 respiration increased by 100% and state 3 respiration, respiratory control ratio and carbonyl cyanide p trifluoromethoxyphenyl hydrazone uncoupled respiration decreased by 46%, 74% and 47% of the controls, respecti The present data suggest that mitochondrial dysfunction may be a very early event in cisplatin induced acute renal failure in rats.
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