DSpace

King Saud University Repository >
King Saud University >
COLLEGES >
Health Colleges >
College of Pharmacy >
College of Pharmacy >

Please use this identifier to cite or link to this item: http://hdl.handle.net/123456789/17890

Title: Effect of captopril on doxorubicin-induced nephrotoxicity in normal rats
Authors: Mansour, MA
El-Kashef, HA
Al-Shabanah, OA
Issue Date: 1999
Abstract: : Biochemical evaluations of the effects of the sulfhydryl-containing angiotensin-converting enzyme inhibitor (captopril) on the nephrotoxicity induced by doxorubicin in normal rats were carried out. A single dose of doxorubicin (15 mg kg(-1)) which caused nephrotoxicity was manifested biochemically by the elevation of serum urea after 24 and 48 h of administration. Also a severe decrease in total proteins and albumin after 4, 24 and 48 h was observed. Moreover, a decrease of non-protein sulfhydryl (-SH) concentrations in the kidney tissues after 24 h and an increase in the lipid peroxidation was observed after 4 h administration of doxorubicin. Captopril (60 mg kg(-1) i.p.) injection did not induce any change in the biochemical parameters measured, however, captopril administered Ih before doxorubicin ameliorated the biochemical toxicity induced by doxorubicin. This was evidenced by a significant reduction in serum urea and the lipid peroxidation after 4 and 24 h and a significant reduction in creatinine after 48 h. Also, the captopril amelioration was evidenced by an increase in total proteins and albumin after 4 and 24 h of doxorubicin administration. Captopril did not change non-protein sulfhydryl (-SH) concentrations or protein content in the kidney tissues. These results suggest that captopril may be beneficial as a protective agent against nephrotoxicity induced by doxorubicin. (C) 1999 The Italian Pharmacological Society.
URI: http://hdl.handle.net/123456789/17890
Appears in Collections:College of Pharmacy

Files in This Item:

File Description SizeFormat
32.doc34 kBMicrosoft WordView/Open

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.

 

DSpace Software Copyright © 2002-2007 MIT and Hewlett-Packard - Feedback