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Cardiovascular Research 1999 42(3):578-582; doi:10.1016/S0008-6363(99)00029-2
© 1999 by European Society of Cardiology
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Copyright © 1999, European Society of Cardiology

Homocysteine and endothelial function

Sagar N. Doshi, Jonathan Goodfellow, Malcolm J. Lewis and Ian F.W. McDowell*

Cardiovascular Sciences Research Group, Wales Heart Research Institute, University of Wales College of Medicine, Heath Park, Cardiff CF4 4XN, UK

mcdowell@cf.ac.uk

* Corresponding author. Tel.: +44-1222-744-851; fax: +44-1222-766-276

Received 12 January 1998; accepted 12 January 1999

The first 150 words of the full text of this article appear below.

See article of Lambert et al. [34] (pages 743–751) in this issue.

The hypothesis that homocysteine may cause vascular disease was originally proposed by McCully, following the observation that premature thromboembolism and atherosclerosis was a feature of homocystinuria [1]. In homocystinuria, a rare inborn error of metabolism, plasma homocysteine concentrations are generally 10 to 50 times that found in the healthy population [2]. This led to the hypothesis that mild to moderate elevations of plasma homocysteine may be a risk factor for atherosclerosis in the general population. This hypothesis has generated considerable interest, particularly as simple therapy with oral B group vitamins significantly lowers plasma homocysteine [3].

Homocysteine is a thiol containing amino acid that is metabolised from methionine, an essential amino acid derived from dietary protein. Homocysteine can be metabolised further to cysteine by transsulfuration (using vitamin B6 as cofactor) or remethylated back to methionine using . . . [Full Text of this Article]


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