Abstract
The pathogenesis of galactose cataract in rat lenses was investigated by measuring changes in bioelectric potential, hydration, ion distribution and kinetics of sodium and potassium movement in cataractous lenses. During initial and vacuolar stages of cataract formation, the potential decreased in parallel with the decrease in concentration of potassium. The latter results primarily from dilution consequent to an increase in hydration. Throughout these stages, concentrations of sodium and chloride in cataractous lenses increased gradually with time on the galactose ration up to the thirteenth day. The concentration of sodium and chloride rose abruptly by the fifteenth day at which time the concentration of potassium fell abruptly. These changes were parallel to the sudden appearance of nuclear cataract and were accompanied by almost total loss of potential reflecting the disappearance of the electrolyte gradient. The rate of efflux of 86Rb (as a substitute for 42K) in cultured lenses of rats maintained on a galactose ration for 3 days was found to increase while the rate of active transport appeared to decrease compared with that of normal lenses. These findings are incompatible with the constant level of potassium found in lenses in situ. That these results might not apply to lenses in vivo because of injury associated with their removal from the globe is discussed in light of experimental evidence showing that the bioelectric potential is reduced by half following excision of the lens from the globe. However, these observations do not preclude the possibility that the rate of active transport of potassium in cataractous lenses in situ had not, in fact, increased. Further studies involving saturation kinetics of potassium transport showed that in rabbit lenses the rate of active transport increases with increasing concentration of intracellular sodium. These observations may provide a rational basis for any possible increased activity in the cation pump in sodium-rich cataractous rat lenses.
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