August 1965
Volume 4, Issue 4
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Articles  |   August 1965
Cation Transport of the Lens
Author Affiliations
  • JOHN E. HARRIS
    Grant B-1979, National Institute of Neurological Diseases and Blindness; Department of Ophthalmology, University of Minnesota Medical School, Minneapolis, Minn.
  • BERNARD BECKER
    Grant B-1979, National Institute of Neurological Diseases and Blindness; Department of Ophthalmology, Washington University School of Medicine, St. Louis, Mo. Supported by Grant B-621, National Institute of Neurological Diseases and Blindness
Investigative Ophthalmology & Visual Science August 1965, Vol.4, 709-722. doi:
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      JOHN E. HARRIS, BERNARD BECKER; Cation Transport of the Lens. Invest. Ophthalmol. Vis. Sci. 1965;4(4):709-722.

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

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Abstract

The lens maintains its cation content by the excretion of sodium and the concentration of potassium. This active transport of cations can be demonstrated in a fairly simple medium. Glucose appears to be the major metabolite supplying energy for transport. The transport of cations demonstrates saturation kinetics and has relatively high Q10 characteristics of active transport systems. Transport can be maintained by anaerobic glycolysis. Of the metabolic inhibitors, transport is most sensitive to iodoacetate. The transport system requires sodium-potassium-activated ATPase as evidenced by sensitivity to ouabain. The major site of transport appears to be across the epithelium of the anterior surface of the lens. It has not been determined whether transport of cations occurs across the fiber membranes.

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