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AbstractDO.05.11 Thioltransferase Glutaredoxin (Grx1) protects lens from oxidative damage induced by UVR-B Meyer L.1,2, Löfgren S.2, Ho Y.3, Lou M.4, Wegener A.2, Holz F.1, Söderberg P.2
1Universitäts-Augenklinik Bonn, Bonn, Deutschland; 2Department of Clinical Neuroscience, Karolinska Insitutet, St Erik's Eye Hospital, Stockholm, Sweden; 3Institute of Environmental Health Sciences and Department of Biochemistry and Molecular Biology, Wayne State University, Detroit, MI, USA; 4Department of Veterinary and Biomedical Sciences, University of Nebraska-Lincoln, Nebraska, USA Objective: To investigate if the Thioltransferase Glutaredoxin 1 (Grx1), a critical protein-thiol repair enzyme, protects the lens from oxidative damage induced by UVR-B exposure in an in vivo cataract model with Grx1-/- and Grx1+/+ mice.
Methods: 36 Grx1-/- mice and Grx1+/+ mice were unilaterally exposed in vivo to UVR type-B for 15 minutes. Groups of 12 animals each received 1.5x, 3x, or 5x UVR-B cataract threshold dose (MTD). 48 hours post UVR-B exposure, the induced cataract was quantified as forward lens light scattering. Based on lens light scattering differences in Grx1-/- and Grx1+/+ mice the relative protection p the Grx1 gene provides against UVR-B induced cataract was derived.
Results: Lens light scattering (tEDC) in Grx1-/- mice was increased in all dose groups compared to lenses with normal Grx1 function (1,5x MTD: 0,24 tEDC vs. 0,2 tEDC; 3x MTD: 0,28 vs. 0,23 tEDC; 5x MTD: 0,3 vs. 0,25 tEDC). The difference was more pronounced with increasing exposure dose. Lens sensitivity for UVR-B induced damage was significantly higher in Grx1-/- lenses compared to Grx1+/+ lenses. The Grx1 gene provides a 44% increase of protection against close to threshold UVR-B induced oxidative stress compared to the absence of the Grx1 gene.
Conclusions: The derived relative protection of 44% the Grx1 gene provides against close to threshold UVR-B demonstrates that Grx1 plays a key role in the protection of lens proteins from acute oxidative stress. Thus Grx1 polymorphisms may cause a varying degree of lens sensitivity to age-related cataract associated oxidative stress.
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