Horm Metab Res 2005; 37(12): 729-733
DOI: 10.1055/s-2005-921093
Original Basic
© Georg Thieme Verlag KG Stuttgart · New York

Influence of Oxygen Concentration on Redox Cycling of Alloxan and Dialuric Acid

H.  J.  Brömme1 , R.  Weinandy2 , E.  Peschke3
  • 1Institute of Pathophysiology, Martin Luther University of Halle-Wittenberg, Germany
  • 2Institute of Zoology, Martin Luther University of Halle-Wittenberg, Germany
  • 3Institute of Anatomy & Cell Biology, Martin Luther University of Halle-Wittenberg, Germany
Further Information

Publication History

Received 25 April 2005

Accepted after revision 5 July 2005

Publication Date:
22 December 2005 (online)

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Abstract

Alloxan, a chemical diabetogen, decays in the absence of reductants into alloxanic acid. In the presence of glutathione, it is reduced via the alloxan radical into dialuric acid, which autoxidizes back to alloxan. During this redox cycling process, reactive oxygen species are formed that destroy β-cells in islets of Langerhans. Previous experiments were conducted with oxygen concentrations about ten times as high as within cells. The aim of our in vitro study was to evaluate the impact of different oxygen concentrations (0, 25, 250 µmol/l) at a given initial ratio of glutathione and alloxan on this redox cycling. Reduction of alloxan, oxidation of glutathione, and the formation of glutathiol (GSSG) were continuously recorded by HPLC for 90 minutes at 25 °C in air, calibration gas, or argon. In the absence of reductants, alloxan irreversibly decomposed into alloxanic acid regardless of oxygen presence. When the reaction system contained glutathione, decomposition was significantly retarded and therefore influenced by oxygen. In argon, decay could not be observed due to its reduction and the absence of oxygen. Increasing oxygen concentration enabled a redox cycling and therefore an ongoing decay. The highest decomposition along with the highest consumption of glutathione occurred at 250 µmol/l oxygen. The lower the oxygen, the more dialuric acid could be detected. After calculation, about 33 redox cycles per hour generates an amount of reactive oxygen species sufficient to damage pancreatic beta cells and induce insulin deficiency.

References

Doz. Dr. rer. nat. habil. Hans-Jürgen Brömme

Institute of Pathophysiology, Martin Luther University of Halle-Wittenberg

Ernst-Grube-Str. 40 · 06097 Halle (Saale) · Germany

Phone: + 49 345 557-4009 ·

Email: h-j.broemme@medizin.uni-halle.de