July 1971
Volume 10, Issue 7
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Articles  |   July 1971
Mechanism of Development of Hereditary Cataract in Mice
Author Affiliations
  • SHUZO IWATA
    Howe Laboratory of Ophthalmology, Harvard Medical School, Massachusetts Eye and Ear Infirmary, 243 Charles Street, Boston, Mass. 02114
  • JIN H. KINOSHITA
    Howe Laboratory of Ophthalmology, Harvard Medical School, Massachusetts Eye and Ear Infirmary, 243 Charles Street, Boston, Mass. 02114
Investigative Ophthalmology & Visual Science July 1971, Vol.10, 504-512. doi:
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      SHUZO IWATA, JIN H. KINOSHITA; Mechanism of Development of Hereditary Cataract in Mice. Invest. Ophthalmol. Vis. Sci. 1971;10(7):504-512.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

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.

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