Nutrients 2013, 5(2), 340-358; doi:10.3390/nu5020340

Selenistasis: Epistatic Effects of Selenium on Cardiovascular Phenotype

1,2email and 2,* email
Received: 14 December 2012; in revised form: 19 January 2013 / Accepted: 23 January 2013 / Published: 31 January 2013
(This article belongs to the Special Issue Dietary Selenium and Health)
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract: Although selenium metabolism is intricately linked to cardiovascular biology and function, and deficiency of selenium is associated with cardiac pathology, utilization of selenium in the prevention and treatment of cardiovascular disease remains an elusive goal. From a reductionist standpoint, the major function of selenium in vivo is antioxidant defense via its incorporation as selenocysteine into enzyme families such as glutathione peroxidases and thioredoxin reductases. In addition, selenium compounds are heterogeneous and have complex metabolic fates resulting in effects that are not entirely dependent on selenoprotein expression. This complex biology of selenium in vivo may underlie the fact that beneficial effects of selenium supplementation demonstrated in preclinical studies using models of oxidant stress-induced cardiovascular dysfunction, such as ischemia-reperfusion injury and myocardial infarction, have not been consistently observed in clinical trials. In fact, recent studies have yielded data that suggest that unselective supplementation of selenium may, indeed, be harmful. Interesting biologic actions of selenium are its simultaneous effects on redox balance and methylation status, a combination that may influence gene expression. These combined actions may explain some of the biphasic effects seen with low and high doses of selenium, the potentially harmful effects seen in normal individuals, and the beneficial effects noted in preclinical studies of disease. Given the complexity of selenium biology, systems biology approaches may be necessary to reach the goal of optimization of selenium status to promote health and prevent disease.
Keywords: selenium; cardiovascular disease; redox balance; methylation; epigenesis; gene expression; heart failure; fibrosis; methionine; homocysteine
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MDPI and ACS Style

Joseph, J.; Loscalzo, J. Selenistasis: Epistatic Effects of Selenium on Cardiovascular Phenotype. Nutrients 2013, 5, 340-358.

AMA Style

Joseph J, Loscalzo J. Selenistasis: Epistatic Effects of Selenium on Cardiovascular Phenotype. Nutrients. 2013; 5(2):340-358.

Chicago/Turabian Style

Joseph, Jacob; Loscalzo, Joseph. 2013. "Selenistasis: Epistatic Effects of Selenium on Cardiovascular Phenotype." Nutrients 5, no. 2: 340-358.

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