Homocysteine, Iron and Cardiovascular Disease: A Hypothesis

Nutrients

Joseph E. Baggott¹ 

[1] Department of Nutrition Sciences, University of Alabama at Birmingham, Birmingham, AL 35294, USA; E-Mail

关键词: iron;    homocysteine;    cardiovascular disease;    methionine;    thioether;   

DOI  :  10.3390/nu7021108

来源: mdpi

【 摘 要 】

Elevated circulating total homocysteine (tHcy) concentrations (hyperhomocysteinemia) have been regarded as an independent risk factor for cardiovascular disease (CVD). However, several large clinical trials to correct hyperhomocysteinemia using B-vitamin supplements (particularly folic acid) have largely failed to reduce the risk of CVD. There is no doubt that a large segment of patients with CVD have hyperhomocysteinemia; therefore, it is reasonable to postulate that circulating tHcy concentrations are in part a surrogate marker for another, yet-to-be-identified risk factor(s) for CVD. We found that iron catalyzes the formation of Hcy from methionine, S-adenosylhomocysteine and cystathionine. Based on these findings, we propose that an elevated amount of non-protein-bound iron (free Fe) increases circulating tHcy. Free Fe catalyzes the formation of oxygen free radicals, and oxidized low-density lipoprotein is a well-established risk factor for vascular damage. In this review, we discuss our findings on iron-catalyzed formation of Hcy from thioethers as well as recent findings by other investigators on this issue. Collectively, these support our hypothesis that circulating tHcy is in part a surrogate marker for free Fe, which is one of the independent risk factors for CVD.

【 授权许可】

CC BY   
© 2015 by the authors; licensee MDPI, Basel, Switzerland.