Mechanism of development of hereditary cataract in mice.

The biochemical evidence regarding a recessively transmitted cataractous trait in mice suggests that an apparent deficiency of Na-K ATPase may be involved in the initiation of this type of cataract. The enzyme defect leads to inefficiency of the cation pump mechanism. This abnormality was demonstrable in 13-day-old mice. At this stage the lens teas clear and the electrolyte levels ivere normal. However, by the twentieth day it became apparent that the defective lens was no longer able to extrude sodium efficiently, therefore sodium content increased. The sudden increase in electrolytes drew water into the lens and an osmotic change occurred. These events preceded the appearance of a "pin-head" nuclear opacity.