gms | German Medical Science

102. Jahrestagung der DOG

Deutsche Ophthalmologische Gesellschaft e. V.

23. bis 26.09.2004, Berlin

Glycosylation of corneal proteins as a protective factor in ageing?

Meeting Abstract

  • corresponding author G. Grütters - Klinik für Ophthalmologie, Universitätsklinikum Schleswig-Holstein, Campus Kiel, Kiel
  • J. A. Reichelt - Klinik für Ophthalmologie, Universitätsklinikum Schleswig-Holstein, Campus Kiel, Kiel
  • B. Nölle - Klinik für Ophthalmologie, Universitätsklinikum Schleswig-Holstein, Campus Kiel, Kiel
  • S. Ritz-Timme - Institut für Rechtsmedizin am UKSH, Campus Kiel, Kiel

Evidenzbasierte Medizin - Anspruch und Wirklichkeit. 102. Jahrestagung der Deutschen Ophthalmologischen Gesellschaft. Berlin, 23.-26.09.2004. Düsseldorf, Köln: German Medical Science; 2004. Doc04dogDO.08.02

Die elektronische Version dieses Artikels ist vollständig und ist verfügbar unter: http://www.egms.de/de/meetings/dog2004/04dog069.shtml

Veröffentlicht: 22. September 2004

© 2004 Grütters et al.
Dieser Artikel ist ein Open Access-Artikel und steht unter den Creative Commons Lizenzbedingungen (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.de). Er darf vervielfältigt, verbreitet und öffentlich zugänglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.


Gliederung

Text

Objective

The extent of aspartic acid racemization of corneal proteins describes ageing processes of the cornea. These are important for transplant quality. Under physiological conditions aspartic acid accumulates age related in proteins of the stroma. As we have shown in previous studies exogenious factors can influence the extent of racemization and consequently the degradation of corneal proteins. In our cornea bank there are many donors having suffered from diabetes mellitus. These donors often reveal high concentrations of glucose in aqueous humour. So the question arises if glycosylation processes may have an impact on corneal proteins.

Methods

The extent of aspartic acid racemization in corneal proteins of donors with known diabetes mellitus and without was evaluated by measurement of D- and L-aspartic acid concentrations using HPLC. Furthermore in vitro-experiments were performed: glucose was added to culture medium in concentrations as it can be found in patients with diabetes. During cultivation endothelium morphology and the extent of aspartic acid racemization in stromal proteins were examined.

Results

In donors with known diabetes the extent of aspartic acid racemization was significantly reduced (p<0.05). In vitro-experiments could show that reduction of endothelial cells in coincidence with cell polymorphism was dependent on glucose concentration. The extent of aspartic acid racemization was lower in those media with added glucose than in routine culture medium.

Conclusions

The evaluation of aspartic acid racemization shows that in diabetes there is diminished corneal protein ageing / degradation. Obviously high glucose concentrations lead to a slower ageing of structure proteins, whereas cellular structures may be damaged.