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Arteriosclerosis, Thrombosis, and Vascular Biology. 2005;25:1532-1535
doi: 10.1161/01.ATV.0000174124.20147.22
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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2005;25:1532.)
© 2005 American Heart Association, Inc.


Editorials

Stored Iron and Vascular Reactivity

Jerome L. Sullivan

From the Department of Pathology, Immunology, and Laboratory Medicine, University of Florida College of Medicine, Gainesville.

Correspondence to Jerome L. Sullivan, MD, PhD, 4475 Old Bear Run, Winter Park, FL 32792. E-mail jlsullivan@pol.net


Key Words: oxidant stress • genetics of cardiovascular disease • endothelium • iron • myeloperoxidase


An extract of the first 250 words of the full text is provided, because this article has no abstract.
 


*    Introduction
 
Zheng et al1 report that volunteer blood donors with a high donation frequency have significantly greater flow-mediated dilation than low frequency donors. Iron status among the frequent donors approximated a state of iron depletion by assessment of conventional iron markers. The study provides important support for the "iron hypothesis," which suggests a protective effect of iron depletion, ie, the absence of storage iron without anemia, against ischemic heart disease.2–4 The blood donor findings suggest a new direction for the study of endothelial iron status in vivo to complement a growing body of work on iron in cultured endothelial cells. In addition, the finding of lower serum nitrotyrosine in frequent donors is consistent with the hypothesis that myeloperoxidase, a powerful emerging cardiovascular risk factor,5–8 is modifiable by manipulation of iron status.

See page 1577


*    Endothelial Iron Status In Vivo
 
In cultured endothelial cells, iron status can be readily manipulated through the use of iron chelators or supplemental iron,9 or by altering the essential fatty acid composition of the culture medium.10 Use of these methods has identified several important effects of iron in endothelial activation and oxidative injury.9,11–20 But the in vitro approach does not define endothelial iron status in vivo, in particular what might represent a physiologically optimal range of endothelial iron concentrations. Iron status parameters such as serum ferritin are imperfect measures of total body iron stores and are likely to be even less adequate in assessing endothelial iron status. There is the additional uncertainty of differences in storage iron concentration in various cell types, . . . [Full Text of this Article]




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