I.
The aims of this project are to delineate the mechanism by which oxidation causes cataract. We shall use the H2O2 model system and study its effect on Na/K ATPase and other transport systems. General metabolism and protein synthesis, protein and lipid structure, proteincalcium interaction, and cell morphology will also be examined. Other model systems for oxidative insult, such as photolysis and high O2 tension, will also be studied. II. Human cataract will be investigated to correlate findings with model systems and to pursue other problems such as disulfide and methionine sulfoxide reduction, the water insoluble and high molecular weight protein, matrix-membrane interactions with high molecular weight protein complexes, covalent crosslinking related to photolysis and polyamines, proteolysis, phosphorylation, H2O2 origin and relationship to ascorbate. III. Drug intervention utilizing model systems.
