Enzymatic studies of cisplatin induced oxidative stress in hepatic tissue of rats

Cisplatin is an active cytotoxic agent that has proved to be successful in the treatment of various types of solid tumors. The drug-induced nephrotoxicity has been very well documented in clinical oncology. However, hepatotoxicity has been rarely characterized and paid attention to, and is the least...

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Published in:European journal of pharmacology Vol. 532; no. 3; pp. 290 - 293
Main Authors: Pratibha, R., Sameer, R., Rataboli, Padmanabh V., Bhiwgade, Dayanand A., Dhume, Chitra Y.
Format: Journal Article
Language:English
Published: Amsterdam Elsevier B.V 27-02-2006
Elsevier
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Summary:Cisplatin is an active cytotoxic agent that has proved to be successful in the treatment of various types of solid tumors. The drug-induced nephrotoxicity has been very well documented in clinical oncology. However, hepatotoxicity has been rarely characterized and paid attention to, and is the least studied. We have used rat as the model to evaluate the effect of cisplatin on liver antioxidant enzymes and to determine whether these modulations in enzymatic activities are involved in hepatotoxicity. Reports obtained from our study indicate that cisplatin increases lipid peroxidation in the treated tissue of rat. The drug is also involved in altering the thiol status of the tissue with concomitant alterations in the enzymatic antioxidants. Glutathione and glutathione reductase levels were significantly decreased after cisplatin therapy, whereas glutathione peroxidase, gamma-glutamyl transpeptidase and catalase showed a significant increase. No statistically significant change was observed in glutathione- S-transferase activity. After cisplatin treatment, cytochrome P 450 showed a significant increase, whereas cytochrome b 5 was decreased. Thus, an alteration in enzymatic antioxidant status with increase in lipid peroxidation indicates that the enzymes play an important role in combating free radical induced oxidative stress on the tissue.
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ISSN:0014-2999
1879-0712
DOI:10.1016/j.ejphar.2006.01.007