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Biomarkers. 2014 Mar;19(2):142-53. doi: 10.3109/1354750X.2014.885084. Epub 2014 Feb 10.

The decrease of NAD(P)H:quinone oxidoreductase 1 activity and increase of ROS production by NADPH oxidases are early biomarkers in doxorubicin cardiotoxicity.

Author information

1
ESTG-Polytechnic Institute of Leiria , Leiria , Portugal .

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.

CONCLUSIONS:

NAD(P)H:

quinone oxidoreductase-1 activity and increase of hydrogen peroxide production by NADPH oxidases are early biomarkers in doxorubicin cardiotoxicity.

PMID:
24506563
DOI:
10.3109/1354750X.2014.885084
[Indexed for MEDLINE]

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