Please use this identifier to cite or link to this item: http://hdl.handle.net/10316/47552
Title: Sub-chronic administration of doxorubicin to Wistar rats results in oxidative stress and unaltered apoptotic signaling in the lung
Authors: Machado, Nuno G 
Baldeiras, Inês 
Pereira, Gonçalo C 
Pereira, Susana P 
Oliveira, Paulo J 
Keywords: Animals; Apoptosis; Body Weight; Caspase 3; Caspase 9; Doxorubicin; Lung; Male; Malondialdehyde; Mitochondrial ADP, ATP Translocases; Oxidative Stress; Rats; Rats, Wistar; Signal Transduction; Time Factors; Toxicity Tests; Tumor Suppressor Protein p53; Vitamin E; Voltage-Dependent Anion Channels; bcl-2-Associated X Protein
Issue Date: 5-Dec-2010
Serial title, monograph or event: Chemico-biological interactions
Volume: 188
Issue: 3
Abstract: Despite the vast published data on cardiac toxicity, there is still little work done regarding the toxicity of the antineoplastic agent Doxorubicin (DOX) in the lung. The aim of the present work was to determine if DOX causes alterations in selected apoptotic proteins and oxidative stress in the lung, in a similar manner to what occurs in the heart. For that purpose, lungs from Wistar-Han rats sub-chronically treated with vehicle or DOX for seven weeks were collected and analyzed concerning several proteins involved in mitochondrial permeabilization and apoptotic pathways, including p53, Bax and Bcl-2 and different oxidative stress markers. After sub-chronic DOX treatment, no alterations in lung proteins involved in mitochondrial membrane permeabilization or caspase 3 and 9-like activities were found. Nevertheless, an increase in malondialdehyde levels and a decrease in the lung concentration of vitamin E were detected, despite no alterations in reduced and oxidized glutathione. The results obtained indicate for the first time that lungs from DOX-treated rats appear to be susceptible to increased lipid peroxidation, which can explain some cases of DOX-induced lung toxicity.
URI: http://hdl.handle.net/10316/47552
DOI: 10.1016/j.cbi.2010.09.027
Rights: openAccess
Appears in Collections:I&D CNC - Artigos em Revistas Internacionais

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