Role of N-Acetylcystein in Protection against Cisplatin Nephrotoxicity | ||||
| Bulletin of Egyptian Society for Physiological Sciences | ||||
| Article 18, Volume 30, Issue 1, December 2010, Page 287-300 PDF (371.31 K) | ||||
| Document Type: Original Article | ||||
| DOI: 10.21608/besps.2010.36179 | ||||
 View on SCiNiTO | ||||
| Authors | ||||
| Sahar Habib* 1; Maggie Ramzy2; Manal Abd Elghany3 | ||||
| 1Forensic Med. And Toxicology Department, Faculty of Medicine, Minia University | ||||
| 2Biochemistry Department, Faculty of Medicine, Minia University | ||||
| 3Pathology Department, Faculty of Medicine, Minia University | ||||
| Abstract | ||||
| Background: Cisplatin (CDDP) is a cytotoxic therapeutic agent that causes many physiological adverse effects such as nephrotoxicity. Although N-acetylcystein (NAC) a thiol containing antioxidant, has been documented to be effective in attenuating CDDP induced renal injury, the precise mechanisms involved in its renoprotection have not been completely clarified. Methods: Four groups of albino rats were used. The first group injected by saline as control, the second by NAC (i.p.), the third by a single bolus of cisplatin (i.v.), and the last by NAC/CDDP, after 5 days from CDDP injection, investigations were conducted on the levels of serum urea and creatinine, oxidant/antioxidant status by estimation of malondialdehyde, catalase and reduced glutathione, and renal and systemic tumor necrosis factor-alpha (TNF-α). Also, renal tissues were examined histopathologically. Results: Administration of cisplatin to rats induced a significant increase in serum urea and creatinine levels in addition to severe alterations in renal tissue architecture. Cisplatin also increased malondialdehyde and decreased glutathione, and catalase in renal tissues. Also, CDDP increased both renal and systemic TNF-α. Administration of NAC markedly reduced the cisplatin-induced higher serum creatinine and urea levels and counteracted the effects of cisplatin on oxidative stress markers, protected the tissues from the cisplatin-induced lipid peroxidation, and increased TNF-α and improved renal tissue architecture. Conclusion: NAC protection is mediated by preventing the decline of antioxidant status, inhibit malondialdehyde and TNF-α and prevent necrosis and apoptosis from kidneys. These results have implications in use of NAC in human application for protecting against drug-induced nephrotoxicity. | ||||
| Keywords | ||||
| Cisplatin; Nephrotoxicity; reduced glutathione; Malondialdehyde; catalase; NAC; TNF- α; apoptosis | ||||
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