The decrease of NAD(P)H:quinone oxidoreductase 1 activity and increase of ROS production by NADPH oxidases are early biomarkers in doxorubicin cardiotoxicity.
Biomarkers
; 19(2): 142-53, 2014 Mar.
Article
em En
| MEDLINE
| ID: mdl-24506563
ABSTRACT
CONTEXT Doxorubicin cardiotoxicity displays a complex and multifactorial progression. OBJECTIVE:
Identify early biochemical mechanisms leading to a sustained imbalance of cellular bioenergetics.METHODS:
Measurements of the temporal evolution of selected biochemical markers after treatment of rats with doxorubicin (20 mg/kg body weight).RESULTS:
Doxorubicin treatment increased lipid oxidation, catalase activity and production of H2O2 by Nox-NADPH oxidases, and down-regulated NAD(P)H quinone oxidoreductase-1 prior eliciting changes in reduced glutathione, protein carbonyls and protein nitrotyrosines. Alterations of mitochondrial and myofibrillar bioenergetics biomarkers were detected only after this oxidative imbalance was established. NAD(P)H quinone oxidoreductase-1 activity and increase of hydrogen peroxide production by NADPH oxidases are early biomarkers in doxorubicin cardiotoxicity.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Doxorrubicina
/
NAD(P)H Desidrogenase (Quinona)
/
Espécies Reativas de Oxigênio
/
Antibióticos Antineoplásicos
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Cardiomiopatias
Limite:
Animals
Idioma:
En
Ano de publicação:
2014
Tipo de documento:
Article