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N. Lassen, J. Bateman, L. Hines, D. Orlicky, J. Piatigorsky, V. Vasiliou; Lens Opacification and Corneal Edema in Aldh1a1(-/-), Aldh3a1(-/-) Single and Double Knockout Mice after UVB Exposure. Invest. Ophthalmol. Vis. Sci. 2007;48(13):2417.
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In most mammalian species ALDH3A1 is expressed at very high concentrations in cornea but is undetectable in lens, whereas ALDH1A1 is expressed at much lower levels in both cornea and lens. We have observed that Aldh3a1(-/-), Aldh1a1(-/-), and Aldh3a1(-/-)/Aldh1a1(-/-) mice develop lens opacification that increases with age. The aim of this study was to test the hypothesis that these proteins protect the eye against UVB-induced corneal injury and cataract formation.
Single and double knockout mice of one month of age were subjected to UVB exposure (302 nm peak wavelength; at 0.05 and 0.2 J/cm2) and structural changes in the cornea and lens were evaluated 12 and 48 hrs after UV-exposure by in vivo slit lamp biomicroscopy and histological analysis. In addition, the chymotrypsin-like activity of the lens 20S proteasome was also determined.
At both UVB doses tested all Aldh genetic stocks exhibited anterior lens subcapsular opacification, which was more pronounced in Aldh3a1(-/-) and Aldh3a1(-/-)/Aldh1a1(-/-)mice. In addition, exposure to high UV dose (0.2 J/cm2) led to the development of corneal edema in all Aldh-defficient micethat was much more pronounced in Aldh3a1(-/-) andAldh3a1(-/-)/Aldh1a1(-/-) mice compared toAldh1a1(-/-) and wild-type animals. Finally, UVB caused significant inhibition of the proteasome activity in all Aldh genetic stocks, especially in Aldh3a1(-/-)/Aldh1a1(-/-) mice.
These data suggest that the corneal ALDH3A1 acts as a UV filter protecting the lens. In addition to other known ALDH3A1 functions (metabolism of lipid peroxidation aldehydes, maintenance of GSH levels and redox balance) our findings establish ALDH3A1 as a major eye ‘safeguard’ that protects the lens and, most likely the retina against UV-induced oxidative damage.
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