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AM Noury, G Heacock, W Watters, J Mellerio, J Marshall; Mechanisms of UV B Cataractogenesis: The Importance of the Lens Epithelium . Invest. Ophthalmol. Vis. Sci. 2002;43(13):3572.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: To determine the primary target and subsequent damage patterns involved in acute UV B cataractogenesis, using an in vitro whole lens model. Methods: Sixty four, aseptically dissected, porcine lenses were randomly assigned to a control group or immediately irradiated with 302nm UV B. 50% of the lenses recieved exposure to the anterior surface and 50% to the posterior surface. Three different exposure doses were used: 0.08J/cm2 (threshold), 0.64J/cm2 (supra-threshold)or 2.56J/cm2 (supra-threshold) for each orientation. All lenses were subsequently cultured in MEM for 10 days. Lens damage was measured daily using a novel scatter meter, consisting of a rotating 650nm diode laser illumination source, light sink and photoresistor. Epithelial/sub-capsular morphological changes were also independently assessed by daily in vivo photomicroscopy and by subsequent histological analysis at day 10(LM and EM). Results: The direction of exposure was independent of the scatter and photomicroscopy changes that developed. Control lenses showed mild transient equatorial opacification on day 1, not manifest in irradiated groups. Lenses exposed to 0.64J/cm2 and 2.56J/cm2 subsequently developed dose-dependent progressive lenticular opacification. The threshold group, in contrast, showed no significant difference from controls. Early in vivo photomicroscopy revealed dose-dependent morphological changes to the anterior aspect of the irradiated lenses but none posteriorly. Posterior damage did occur at later stages in the opacifying suprathreshold groups but this but this was always following marked anterior damage. Histology revealed gross anterior epithelial and adjacent lens fibre cell damage but only in the supra-threshold doses. Conclusion: This data collectively suggests that the anterior epithelium is the primary target in acute UVB cataractogenesis. Threshold doses transiently affect the epithelial pump but do not progress to permanent opacification. Higher supra-thresold doses cause progressive cataractogenesis, with evidence of cell death and progressive secondary lens fibre damage. This has relevance for managing UV cataract risk.
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