Ultraviolet light and human lens pigmentation.
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Biomedical subjects
Publications and source records attributed to S Zigman.
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Variations in size and charge of calf lens proteins, particularly gamma crystallins, were studied by polyacrylamide gel electrophoresis. Exposure of gamma crystallins to near-UV light in the presence of L-tryptophan produces species of higher electrophoretic mobility and higher retardation. Treatment with urea and sulfonation also produced changes in the retardation co-efficient. The increase of retardation co-efficient of gamma crystallin is interpreted to be a result of conformational changes. Gamma crystallins are particularly sensitive to photo-modification, and this process may be associated with age-related changes in the lens.
Certain ocular proteins have been found to be chemically modified by exposure to near-UV light (320-390 nm) in the presence of tryptophan. Colored and fluorescent tryptophan photoproducts bind firmly to proteins, thereby altering their physico-chemical properties. The question of whether such a reaction would inhibit the catalytic action of catalase is herein raised. When solutions of bovine liver catalase were re-incubated up to 24 hr under near-UV with preirradiated tryptophan and dialyzed, most of the ability of the enzyme to decompose H2O2 was lost. Similar results occurred for catalase activities of bovine cornea and lens epithelia. The enzyme protein exhibited altered UV absorption and fluorescence spectra and increased electrophoretic mobility after binding photoproducts, Near-UV light photoproducts of tryptophan are thus capable of deactivating crystalline and tissue catalase.
Exposure of dilute aqueous solutions of tryptophan to near UV light (320 to 390 nm) at subsolar levels yields fluorescent photoproducts capable of inhibiting the growth and differentiation of cultured mouse embryonic fibroblasts and fertilized sea urchin eggs. The ability of these cells to incorporate labelled precursors of protein, RNA, and DNA into their respective macromolecules was markedly inhibited by adding tryptophan preirradiated with near UV light to their incubation media. Thus the inhibition of growth and differentiation of these cells seems to result from a depression of their ability to synthesize macromolecules in the presence of the photoproducts.
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Albino inbred mice (A/J strain exposed to 40-w black light fluorescent lamps (BLB) for 12 hr a day for up to a year developed inflammatory and hyperplastic responses on hairless ear and tail skin, but not on back skin covered by hair. After 1 year of such exposure, many individuals developed papillomas, carcinomas, and sarcomas on their ears and tails. It may be concluded that black light is a skin carcinogen for A/J mice.
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Continuous exposure of mice to near-ultraviolet (UV) light (black light) over a period of 19 weeks induces adverse alterations in lens protein chemistry, in lens epithelial cell differentiation, and in retinal photoreceptor structure at more than a doubled rate as for 12 hours a day of intermittent exposure. No histologic changes were found in the cornea. The results may indicate the presence of repair mechanisms in these ocular tissues for damage induced by radiant energy.
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