More than 30 years ago, the initial changes in lens biochemistry associated with age-onset cataract formation were described. In the past decade, however, little additional data pertaining to this process has been gathered due to a lack of human cataracts to study. A common property of aged human lens is the accumulation of yellow chromophores, which are bound to proteins. These modifications can absorb UVA light and lead to the formation of reactive oxygen species in vitro. This is important because the amount of UVA light impingement on the human lens in situ is a thousand times greater than UVB, and all of it is absorbed within the lens. The chromophores responsible for this yellowing will be isolated from aged human lenses and cataracts and their photochemistry studied. Since it seems likely that there is little or no oxygen in the human lens, much of this photochemistry will involve the reactivity of the activated free radicals formed by UVA light in argon-saturated solutions. These effects may include loss of antioxidants, inactivation of enzymes which protect the lens and protein crosslinking. This grant, while dealing solely with UVA affects on lens tissue, still carries the name from 24 years ago.
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