Volume 21, Issue 4 (Mars 1997)
Research in Medicine 1997, 21(4): 17-26 |
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Ahvaz University of Medical Seiences & Health Services,Iran.
Abstract: (1766 Views)
SUMMARY
Cisplatin is a widely used anticancer agents that is effective against ovarian and other tumors. This drug is recognized as nephrotoxic in human and experimental animals. The effect of cisplatin-induced kidney injury was predominantly investigated in male animals. This study was designed to assess effects of cisplatin on male and female rat kidneys. We also investigated the effect of glutathione (GSH) on cisplatin nephrotoxicity. Adult male and female rats were given a single ip administration of either cisplatin (5 mg/kg) or vehicle (normal saline). Another series of animals were treated ip with 300 mg/kg GSH or vehicle (normal saline) 30 min prior to administration of cisplatin (5 mg/kg) or normal saline. All animals were killed 5 days later. Nephrotoxicity were evaluated by using BUN, serum creatinine values and kidney histopathological examination. BUN and serum creatinine significantly increased in cisplatin treated animals when compared to those of controls. However this drug produced the same degree of BUN and creatinine elevations in both male and female rats. Histopathologically, cisplatin induced injury in renal proximal tubular cells. Pretreatment of animals with GSH significantly decreased cisplatin nephrotoxicity. The results of this study demonstrated that cisplatin produced kidney injury in both sexes of rats and GSH protects animals against cisplatin nephrotoxicity.
Cisplatin is a widely used anticancer agents that is effective against ovarian and other tumors. This drug is recognized as nephrotoxic in human and experimental animals. The effect of cisplatin-induced kidney injury was predominantly investigated in male animals. This study was designed to assess effects of cisplatin on male and female rat kidneys. We also investigated the effect of glutathione (GSH) on cisplatin nephrotoxicity. Adult male and female rats were given a single ip administration of either cisplatin (5 mg/kg) or vehicle (normal saline). Another series of animals were treated ip with 300 mg/kg GSH or vehicle (normal saline) 30 min prior to administration of cisplatin (5 mg/kg) or normal saline. All animals were killed 5 days later. Nephrotoxicity were evaluated by using BUN, serum creatinine values and kidney histopathological examination. BUN and serum creatinine significantly increased in cisplatin treated animals when compared to those of controls. However this drug produced the same degree of BUN and creatinine elevations in both male and female rats. Histopathologically, cisplatin induced injury in renal proximal tubular cells. Pretreatment of animals with GSH significantly decreased cisplatin nephrotoxicity. The results of this study demonstrated that cisplatin produced kidney injury in both sexes of rats and GSH protects animals against cisplatin nephrotoxicity.
Type of Study: Original |
Subject:
Microbiology
Received: 2020/02/22 | Accepted: 2020/02/22 | Published: 2020/02/22
Received: 2020/02/22 | Accepted: 2020/02/22 | Published: 2020/02/22
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