Mechanism of Development of Hereditary Cataract in Mice

¹ Howe Laboratory of Ophthalmology, Harvard Medical School, Massachusetts Eye and Ear Infirmary, 243 Charles Street, Boston, Mass. 02114

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 were normal. However, by the twentieth day it became apparent that the defective lens was no longer ableto extrude sodium efficiently, therefore sodium content increased. The sudden increase in electrolytes drew water into thelens and an osmotic change occurred. These events preceded the appearance of a "pin-head" nuclear opacity.

Key Words: hereditary mouse cataracts • lens Na-K ATPase deficiency • cataracts • lens electrolyte changes • lens cation pump defect

Submitted on June 1, 1971
Accepted on June 11, 1971

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