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Study of toxic effects on hearing, kidney and liver of mice induced by anticancer agent of cisplatin and their mechanisms

Liao Ying

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Abstract

AIM To establish an animal experimental model for study on prevention of cisplatin toxicity and explore the possible mechanisms of the toxicity induced by cisplatin administration. METHODS Cisplatin was administered i.p consecutively for five days to male mice weighted from 28 to 30 g. The toxic effects induced by different doses of cisplatin on hearing, liver and kidney were determined. RESULTS Dose dependent decrease of body weight, abnormality of kidney and liver coefficients, levels of BUN and activities of ALT in serum were induced by cisplatin administration. Furthermore, Levels of GSH, activities of GSH Px and SOD increased significantly in kidney. Reversely, levels of GSH, activities of GSH Px and SOD in liver decreased and levels of LPO increased significantly in animals given cisplatin compared with those in control animals. CONCLUSION Obvious damage on hearing, liver and kidney of mice could be induced after consecutively 5 days administration of cisplatin with doses range from 3 0 to 4 0 mg·kg -1 (body weight). Oxidative damage is one of the mechanisms of these toxic effects on liver and kidney induced by cisplatin. But for different organs or at different stages of cisplatin administration, the main mechanism may be different.

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AIM To establish an animal experimental model for study on prevention of cisplatin toxicity and explore the possible mechanisms of the toxicity induced by cisplatin administration. METHODS Cisplatin was administered i.p consecutively for five days to male mice weighted from 28 to 30 g. The toxic effects induced by different doses of cisplatin on hearing, liver and kidney were determined. RESULTS Dose dependent decrease of body weight, abnormality of kidney and liver coefficients, levels of BUN and activities of ALT in serum were induced by cisplatin administration. Furthermore, Levels of GSH, activities of GSH Px and SOD increased significantly in kidney. Reversely, levels of GSH, activities of GSH Px and SOD in liver decreased and levels of LPO increased significantly in animals given cisplatin compared with those in control animals. CONCLUSION Obvious damage on hearing, liver and kidney of mice could be induced after consecutively 5 days administration of cisplatin with doses range from 3 0 to 4 0 mg·kg -1 (body weight). Oxidative damage is one of the mechanisms of these toxic effects on liver and kidney induced by cisplatin. But for different organs or at different stages of cisplatin administration, the main mechanism may be different.

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Available abstract

AIM To establish an animal experimental model for study on prevention of cisplatin toxicity and explore the possible mechanisms of the toxicity induced by cisplatin administration. METHODS Cisplatin was administered i.p consecutively for five days to male mice weighted from 28 to 30 g. The toxic effects induced by different doses of cisplatin on hearing, liver and kidney were determined. RESULTS Dose dependent decrease of body weight, abnormality of kidney and liver coefficients, levels of BUN and activities of ALT in serum were induced by cisplatin administration. Furthermore, Levels of GSH, activities of GSH Px and SOD increased significantly in kidney. Reversely, levels of GSH, activities of GSH Px and SOD in liver decreased and levels of LPO increased significantly in animals given cisplatin compared with those in control animals. CONCLUSION Obvious damage on hearing, liver and kidney of mice could be induced after consecutively 5 days administration of cisplatin with doses range from 3 0 to 4 0 mg·kg -1 (body weight). Oxidative damage is one of the mechanisms of these toxic effects on liver and kidney induced by cisplatin. But for different organs or at different stages of cisplatin administration, the main mechanism may be different.

Key concepts: Cisplatin, Ototoxicity, Toxicity, Kidney, Pharmacology, Glutathione, Nephrotoxicity, Medicine

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