Document Detail


Both selenium deficiency and modest selenium supplementation lead to myocardial fibrosis in mice via effects on redox-methylation balance.
MedLine Citation:
PMID:  23097236     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
SCOPE: Selenium has complex effects in vivo on multiple homeostatic mechanisms such as redox balance, methylation balance, and epigenesis, via its interaction with the methionine-homocysteine cycle. In this study, we examined the hypothesis that selenium status would modulate both redox and methylation balance and thereby modulate myocardial structure and function.
METHODS AND RESULTS: We examined the effects of selenium-deficient (<0.025 mg/kg), control (0.15 mg/kg), and selenium-supplemented (0.5 mg/kg) diets on myocardial histology, biochemistry and function in adult C57/BL6 mice. Selenium deficiency led to reactive myocardial fibrosis and systolic dysfunction accompanied by increased myocardial oxidant stress. Selenium supplementation significantly reduced methylation potential, DNA methyltransferase activity and DNA methylation. In mice fed the supplemented diet, inspite of lower oxidant stress, myocardial matrix gene expression was significantly altered resulting in reactive myocardial fibrosis and diastolic dysfunction in the absence of myocardial hypertrophy.
CONCLUSION: Our results indicate that both selenium deficiency and modest selenium supplementation leads to a similar phenotype of abnormal myocardial matrix remodeling and dysfunction in the normal heart. The crucial role selenium plays in maintaining the balance between redox and methylation pathways needs to be taken into account while optimizing selenium status for prevention and treatment of heart failure.
Authors:
Nicole Metes-Kosik; Ivan Luptak; Patricia M Dibello; Diane E Handy; Shiow-Shih Tang; Hui Zhi; Fuzhong Qin; Donald W Jacobsen; Joseph Loscalzo; Jacob Joseph
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2012-10-24
Journal Detail:
Title:  Molecular nutrition & food research     Volume:  56     ISSN:  1613-4133     ISO Abbreviation:  Mol Nutr Food Res     Publication Date:  2012 Dec 
Date Detail:
Created Date:  2012-12-11     Completed Date:  2013-05-30     Revised Date:  2013-12-04    
Medline Journal Info:
Nlm Unique ID:  101231818     Medline TA:  Mol Nutr Food Res     Country:  Germany    
Other Details:
Languages:  eng     Pagination:  1812-24     Citation Subset:  IM    
Copyright Information:
© 2012 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.
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MeSH Terms
Descriptor/Qualifier:
Animals
Cardiomyopathies / drug therapy*,  physiopathology
Cysteine / blood
DNA Methylation / drug effects*
Diet
Dietary Supplements*
Epigenomics
Fibrosis
Glutathione / blood
Homocysteine / blood
Isoprostanes / blood
Male
Mice
Mice, Inbred C57BL
Myocardium / pathology*
Oxidative Stress / drug effects*
Real-Time Polymerase Chain Reaction
Selenium / blood,  deficiency*,  pharmacology*
Selenoproteins / genetics,  metabolism
Grant Support
ID/Acronym/Agency:
HL107192/HL/NHLBI NIH HHS; HL108630/HL/NHLBI NIH HHS; HL48743/HL/NHLBI NIH HHS; HL52234/HL/NHLBI NIH HHS; HL61795/HL/NHLBI NIH HHS; HL70819/HL/NHLBI NIH HHS; HL89734/HL/NHLBI NIH HHS; P01 HL048743/HL/NHLBI NIH HHS; P50 HL107192/HL/NHLBI NIH HHS; R01 HL052234/HL/NHLBI NIH HHS; R21 HL089734/HL/NHLBI NIH HHS; R37 HL061795/HL/NHLBI NIH HHS; U01 HL108630/HL/NHLBI NIH HHS; U54 HL070819/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Isoprostanes; 0/Selenoproteins; 0LVT1QZ0BA/Homocysteine; GAN16C9B8O/Glutathione; H6241UJ22B/Selenium; K848JZ4886/Cysteine
Comments/Corrections

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