Forschungs- & Entwicklungsinformationsdienst der Gemeinschaft - CORDIS

Vascular endothelial cells are activated by EDTA chelation therapy

Ethylenediamine-tetraacetic acid (EDTA) chelation therapy is practiced as an alternative treatment for coronary artery disease, believing that removal of metal ions like copper and iron by EDTA is able to prevent atherogenic oxidative stress. Little is known, however, on its biological effects on vascular endothelium. In this study, we examined the effects of metal chelation with EDTA on the expression of endothelial ICAM-1, VCAM-1 and E-selectin as well as the adhesion of monocytes to the endothelium, being a crucial event in atherogenesis.

In a serum free condition, addition of EDTA enhanced, rather than reversed, iron-induced endothelial adhesion molecule expression. In the presence of copper, EDTA induced ICAM-1 expression. In 50% human pooled serum, EDTA alone, without added iron or copper, enhanced the expression of adhesian molecules. EDTA appeared to promote accumulation of intracellular labile iron, inducing oxygen radical mediated endothelial cell activation.

This activation could be reversed by deferoxamine or deferiprone, two iron chelators widely used for the treatment of secondary iron overload. High doses vitamin C, routinely added to EDTA therapy, augmented rather than reversed EDTA effects, and moreover inducing monocyte adherence to vascular endothelium. Endothelial activation by EDTA-vitamin-C treatment, following interaction with transition metal iron, therefore, may cause harmful effects when being used for the treatment of coronary artery disease.

Conclusion: In particular subjects with iron overload could be at risk after EDTA chelation therapy.

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