Epidemiological data supports lead exposure as a risk factor for cataract development. Previous studies which demonstrated oxidative imbalances in the lens following in vivo Pb2+ exposure support the idea that lead exposure can alter the lens biochemical homeostasis which may ultimately lead to loss of lens clarity with time. α-Crystallin, a major lens structural protein and molecular chaperone, undergoes various post-translational modifications upon aging which may contribute to decreased chaperone function and contribute to loss of lens clarity. This study evaluated the impact of 5 weeks of oral Pb2+ exposure (peripheral Pb2+ level ∼30 μg/dL) on the αA-crystallin protein profile of the lens from Fisher 344 rats. Decreases in relative protein spot intensity of more acidic forms of αA- and βA4-crystallin and of truncated forms of αA-crystallin were noted. This data indicates that changes in post-translational processing of crystallins do occur in vivo following short courses of clinically relevant Pb2+-exposure. In addition, organ culture of lenses from 4.5-month-old rats in 5 μM Pb2+ resulted in opacities, demonstrating that lead is toxic to the lens and can induce a loss of lens clarity.
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