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Title: Roles of oxidative stress and Akt signaling in doxorubicin cardiotoxicity

Journal Article · · Biochemical and Biophysical Research Communications
 [1];  [2];  [3];  [3];  [4];  [4];  [4]
  1. Department of Human Functional Genomics, Life Science Research Center, Mie University, 1577 Kurimamachiya-cho, Tsu, Mie 514-8507 (Japan) and Social Life Science, Nagoya University Graduate School of Medicine, Nagoya (Japan)
  2. Department of Human Functional Genomics, Life Science Research Center, Mie University, 1577 Kurimamachiya-cho, Tsu, Mie 514-8507 (Japan)
  3. Laboratory of Food and Biodynamics, Graduate School of Bioagricultural Sciences, Nagoya University, Nagoya (Japan)
  4. Social Life Science, Nagoya University Graduate School of Medicine, Nagoya (Japan)

Cardiotoxicity is a treatment-limiting side effect of the anticancer drug doxorubicin (DOX). We have now investigated the roles of oxidative stress and signaling by the protein kinase Akt in DOX-induced cardiotoxicity as well as the effects on such toxicity both of fenofibrate, an agonist of peroxisome proliferator-activated receptor-{alpha}, and of polyethylene glycol-conjugated superoxide dismutase (PEG-SOD), an antioxidant. Mice injected intraperitoneally with DOX were treated for 4 days with fenofibrate or PEG-SOD. Fenofibrate and PEG-SOD each prevented the induction of cardiac dysfunction by DOX. Both drugs also inhibited the activation of the transcription factor NF-{kappa}B and increase in lipid peroxidation in the left ventricle induced by DOX, whereas only PEG-SOD inhibited the DOX-induced activation of Akt and Akt-regulated gene expression. These results suggest that fenofibrate and PEG-SOD prevented cardiac dysfunction induced by DOX through normalization of oxidative stress and redox-regulated NF-{kappa}B signaling.

OSTI ID:
20991443
Journal Information:
Biochemical and Biophysical Research Communications, Vol. 359, Issue 1; Other Information: DOI: 10.1016/j.bbrc.2007.05.027; PII: S0006-291X(07)00982-5; Copyright (c) 2007 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
Country of Publication:
United States
Language:
English