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

Please use this identifier to cite or link to this item: http://hdl.handle.net/123456789/6180

Title: Alpha-Lipoic Acid Ameliorates Myocardial Toxicity Induced By Doxorubicin
Authors: Al-Majed, Abdulhakeem A.
Gado, Ali M.
Al-Shabanah, Othman A.
Mansour, Mahmoud A.
Keywords: Doxorubicin
Lactate dehydrogenase
Creatine phosphokinase
Alpha-lipoic acid
Lipid peroxidation
Reduced glutathione
Issue Date: 21-Nov-2002
Publisher: Elsevier Science and Ideal Library
Citation: Pharmacological Research: 46(6); 499-503
Abstract: The effect of alpha-lipoic acid (LA) on the cardiotoxicity induced by doxorubicin (DOX) was investigated. A single dose of DOX (15 mg kg−1, i.p) induced cardiotoxicity manifested biochemically by a significant elevation of serum creatine phosphokinase (CK; EC: and lactate dehydrogenase (LDH; EC: 48 h later. Moreover, cardiotoxicity was further confirmed by the significant increase in lipid peroxides measured as malondialdehyde (MDA), and significant decrease in protein thiols (Protein-SH) content in heart tissues. Administration of LA (100 mg kg−1) orally for 5 days before and 2 days after DOX injection produced a significant protection against cardiotoxicity induced by DOX. The amelioration of cardiotoxicity was evident by significant reductions in serum CK and LDH. Moreover, LA prevented the rise of MDA as well as the significant reduction of Protein-SH. These results may suggest that LA has a protective effect against cardiotoxicity induced by DOX and it may, therefore, improve the therapeutic index of DOX.
URI: http://hdl.handle.net/123456789/6180
Appears in Collections:College of Pharmacy

Files in This Item:

File Description SizeFormat
Alpha-Lipoic Acid Ameliorates Myocardial Toxicity Induced By Doxorubicin.pdfpdf85.98 kBAdobe PDFView/Open

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


DSpace Software Copyright © 2002-2009 MIT and Hewlett-Packard - Feedback