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Homocysteine Levels, Paraoxonase 1 (PON1) Activity, and Cardiovascular Risk
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To the Editor: Dr Bhattacharyya and colleagues1 described a strong link between genetic determinants and activity of paraoxonase 1 (PON1), oxidative stress, all-cause mortality, and major adverse coronary events. The authors suggested that their findings support the hypothesis that fewer oxidized lipids in the low-density lipoprotein cholesterol particle would be of clinical benefit, an idea for which I am not aware of any trial support.
The suggested mechanistic link is not as clear-cut as the authors imply, and other mechanisms can contribute to the protective role of PON1. Although the notion that PON1 has an antioxidant function is assumed, I know of no biochemical basis for that function. It seems unlikely that the paraoxonase or arylesterase activities measured are related to the suggested antioxidative function of PON1; paraoxon and phenylacetate are artificial substrates,1-2 convenient for monitoring hydrolytic activity of PON1, which is not a putative redox activity.
However, there is . . . [Full Text of this Article]
Eddie Vos, MEng
vos@health-heart.org
Sutton, Quebec, Canada
RELATED ARTICLE
Relationship of Paraoxonase 1 (PON1) Gene Polymorphisms and Functional Activity With Systemic Oxidative Stress and Cardiovascular Risk
Tamali Bhattacharyya, Stephen J. Nicholls, Eric J. Topol, Renliang Zhang, Xia Yang, David Schmitt, Xiaoming Fu, Mingyuan Shao, Danielle M. Brennan, Stephen G. Ellis, Marie-Luise Brennan, Hooman Allayee, Aldons J. Lusis, and Stanley L. Hazen
JAMA. 2008;299(11):1265-1276.
ABSTRACT
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RELATED LETTER
Homocysteine Levels, Paraoxonase 1 (PON1) Activity, and Cardiovascular Risk—Reply
Stephen J. Nicholls and Stanley L. Hazen
JAMA. 2008;300(2):169.
EXTRACT
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