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Original Paper

Stimulation of Suicidal Erythrocyte Death by Methylglyoxal

Nicolay J.P.1 · Schneider J.1 · Niemoeller O.M.1 · Artunc F.1 · Portero-Otin M.2 · Haik Jr. G.3 · Thornalley P.J.2 · Schleicher E.4 · Wieder T.1 · Lang F.1

Author affiliations

1Department of Physiology, and 4Department of Internal Medicine, University of Tübingen, 2Department of Biological Sciences, University of Essex, 3George Haik Eye Clinic, New Orleans, Louisiana

Corresponding Author

Prof. Dr. Florian Lang

Physiologisches Institut der Universität Tübingen

Gmelinstr. 5, D-72076 Tübingen (Germany)

Tel. +49 7071 29 72194, Fax: +49 7071 29 5618

E-Mail florian.lang@uni-tuebingen.de

Related Articles for ""

Cell Physiol Biochem 2006;18:223–232

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Diabetes increases the percentage of circulating erythrocytes exposing phosphatidylserine (PS) at the cell surface. PS-exposing erythrocytes are recognized, bound, engulfed and degraded by macrophages. Thus, PS exposure, a feature of suicidal erythrocyte death or eryptosis, accelerates clearance of affected erythrocytes from circulating blood. Moreover, PS-exposing erythrocytes bind to the vascular wall thus interfering with microcirculation. The present study explored mechanisms involved in the triggering of PS exposure by methylgloxal, an extra- and intracellular metabolite which is enhanced in diabetes. PS exposure, cell size and cytosolic Ca2+-activity after methylglyoxal treatment were measured by FACS analysis of annexin V binding, forward scatter and Fluo-3-fluorescence, respectively, and it was shown that the treatment significantly enhanced the percentage of PS-exposing erythrocytes at concentrations (0.3 µM) encountered in diabetic patients. Surprisingly, methylglyoxal did not significantly increase cytosolic Ca2+ concentration, and at concentrations up to 3 µM, did not decrease the forward scatter. Instead, exposure to methylglyoxal inhibited glycolysis thus decreasing ATP and GSH concentrations. In conclusion, methylglyoxal impairs energy production and anti-oxidative defense, effects contributing to the enhanced PS exposure of circulating erythrocytes and eventually resulting in anemia and deranged microcirculation.

Article / Publication Details

First-Page Preview
Abstract of Original Paper

Published online: November 29, 2006
Issue release date: January 2006

Number of Print Pages: 10
Number of Figures: 0
Number of Tables: 0

ISSN: 1015-8987 (Print)
eISSN: 1421-9778 (Online)

For additional information: https://www.karger.com/CPB

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