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L.M. Meyer, J. Bergmanson, X. Dong, V. Mody, M. Kakar, S. Löfgren, A. Wegener, F.G. Holz, P. Söderberg; Acute Cataract and Repair in the Mouse Lens Following UVR–B Exposure . Invest. Ophthalmol. Vis. Sci. 2006;47(13):4080.
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© ARVO (1962-2015); The Authors (2016-present)
To investigate cataract evolution, lens epithelial damage and epithelial repair following unilateral in vivo exposure to double threshold dose UVR–B in the C57BL/6 mouse lens.
A total of 20 six weeks old female mice were divided into four latency groups. The animals received in vivo double threshold dose (MTD2.3:16) 6.4 kJ/m2 UVR–B for 15 minutes. The radiation output of the UVR– source had MAX at 302.6 nm with 4.5 nm [FWHM]. At days 1, 2, 4, and 8 after exposure, animals were sacrificed and light scattering in the exposed and the contralateral not exposed lenses was measured quantitatively. Evolution of cataract morphology was documented using grid and dark field illumination photography. Damage to the lens epithelium and the anterior cortex was investigated with; light microscopy in toluidine blue stained semithin sections , transmission electron microscopy (TEM) and scanning electron microscopy (SEM).
One day after exposure to UVR–B, lenses developed anterior subcapsular, and/ or cortical and nuclear cataract. Over latency times 2, 4, and 8 days, subcapsular cataract was organized in an annulus that shrank towards the anterior pole. Lens epithelial cell damage was seen in TEM as apoptotic cells, apoptotic bodies, nuclear chromatin condensation, and swollen and disrupted anterior cortex fibers. TEM and light microscopy confirmed the movement of apoptotic bodies and damaged cells from the equator towards the anterior sutures. Four days following UVR–B exposure the single layered epithelium had transformed at damaged sites into a multilayered epithelial wall that moved towards the anterior pole with. Contralateral unexposed lenses were clear and did not present the multilayered pattern.
UVR–B induced cataract in the mouse is repaired by retrograde epithelial cell and cell debris movement towards the anterior pole, thus in centripetal and opposite direction to regular epithelial cell differentiation.
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