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Published on: February 25, 2016
Gene expression of antioxidative enzymes in the human heart: increased expression of catalase in the end-stage
S Dieterich1, U Bieligk, K Beulich
1Department of Cardiology and Angiology, University Freiburg, Freiburg, Germany.
Circulation
|January 5, 2000
Summary
Oxidative stress in heart failure increases catalase gene expression as a compensatory mechanism. Manganese superoxide dismutase (MnSOD), copper-zinc superoxide dismutase (CuZnSOD), and glutathione peroxidase (GPX) gene expression remained unchanged in failing hearts.
Area of Science:
- Cardiology
- Molecular Biology
- Biochemistry
Background:
- Oxidative stress is implicated in heart failure pathogenesis.
- Gene expression of reactive oxygen metabolite-metabolizing enzymes in the human heart is not well understood.
Purpose of the Study:
- To investigate the gene expression of key antioxidant enzymes in human end-stage heart failure.
- To determine if oxidative stress leads to specific changes in antioxidant enzyme expression.
Main Methods:
- Analyzed mRNA and protein levels of MnSOD, CuZnSOD, GPX, and catalase in myocardial tissue from nonfailing and failing human hearts (dilated and ischemic cardiomyopathy).
- Utilized Northern blot, Western blot, and ELISA techniques.
- Assessed enzyme activities for MnSOD, CuZnSOD, GPX, and catalase.
Main Results:
- Catalase mRNA and protein levels were significantly upregulated in both dilated cardiomyopathy (DCM) and ischemic cardiomyopathy (ICM) hearts compared to controls.
- Increased catalase enzyme activity was observed in failing hearts, correlating with elevated mRNA and protein levels.
- mRNA and protein levels, as well as enzyme activities, of MnSOD, CuZnSOD, and GPX were not significantly different between failing and nonfailing hearts.
Conclusions:
- Human end-stage heart failure exhibits specific upregulation of catalase gene expression.
- This catalase upregulation may serve as a compensatory mechanism against increased oxidative stress.
- Gene expression of SOD and GPX remains unaffected in failing human hearts.

