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L. M. Meyer, S. Löfgren, Y.-S. Ho, A. Wegener, X. Dong, V. Mody, M. Kakar, F. G. Holz, P. G. Söderberg; Delayed Cataract Repair and Increased Lens Light Scattering in Glrx1 Knockout Mice Following Exposure to UVR-B. Invest. Ophthalmol. Vis. Sci. 2007;48(13):2419.
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To investigate cataract evolution and cataract repair following unilateral in vivo exposure to above threshold doses UVR-B in Glutaredoxin 1 (Glrx1) homozygous knockout mice (Glrx1 -/-) and genetically matched wild type mice (Glrx1+/+).
A total of 30 six weeks old homozygous Glrx1 knockout mice (Glrx1-/-) and 30 age matched Glrx1 wild type mice (Glrx1+/+) were unilaterally exposed in vivo to UVR-B for 15 minutes. The radiation output of the UVR- source had MAX at 302.6 nm with 4.5 nm [FWHM]. The animals received 1.5/ 3/or 5 times threshold dose (MTD2.3:16) UVR-B depending on dose group (n=10). 48 hours following UVR - B exposure Glrx1 knockout and Glrx1 wildtype mice were sacrificed. Experimentally induced cataract was quantified as lens light scattering in the exposed and the contralateral not exposed lenses with a light dissemination meter (LDM meter). Evolution of cataract morphology was documented using grid and dark field illumination photography.
Exposed lenses of Glrx1 knockout and wildtype mice developed anterior subcapsular cataract 48 hours after exposure to UVR-B. Light scattering in Glrx1-/- lenses was increased in all dose groups (1.5 MTD/ 3 MTD/ 5 MTD) as compared to lenses with normal Glutaredoxin 1 function. With increasing UVR-B dose cataract in Glrx1-/- mice extended radially further towards the lens equator 48 hours post-exposure than in wild type animals. Furthermore anterior subcapsular cataract in knockout mice was less demarcated from clear lens areas compared to (Glrx1+/+) mice lenses.
Glrx1-/- knockout mice lenses are more susceptible to oxidative stress induced by UVR-B exposure than lenses with normal Glrx1 function. Furthermore the inactivation of Glrx1 delays lens epithelial cell repair.
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