December 1969
Volume 8, Issue 6
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Articles  |   December 1969
Changes in the levels of free amino acids and myo-inositol in the galactose-exposed lens
Author Affiliations
  • J. H. KINOSHITA
    Howe Laboratory of Ophthalmology, Harvard Medical School, the Massachusetts Eye and Ear Infirmary Boston, Mass. Wills Eye Hospital and Research Institute Philadelphia, Pa.
  • G. W. BARBER
    Howe Laboratory of Ophthalmology, Harvard Medical School, the Massachusetts Eye and Ear Infirmary Boston, Mass. Wills Eye Hospital and Research Institute Philadelphia, Pa.
  • L. O. MEROLA
    Howe Laboratory of Ophthalmology, Harvard Medical School, the Massachusetts Eye and Ear Infirmary Boston, Mass. Wills Eye Hospital and Research Institute Philadelphia, Pa.
  • B. TUNG
    Howe Laboratory of Ophthalmology, Harvard Medical School, the Massachusetts Eye and Ear Infirmary Boston, Mass. Wills Eye Hospital and Research Institute Philadelphia, Pa.
Investigative Ophthalmology & Visual Science December 1969, Vol.8, 625-632. doi:
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      J. H. KINOSHITA, G. W. BARBER, L. O. MEROLA, B. TUNG; Changes in the levels of free amino acids and myo-inositol in the galactose-exposed lens. Invest. Ophthalmol. Vis. Sci. 1969;8(6):625-632.

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Abstract

Studies of the effects of galactose on the lens have revealed that marked depressions in the levels of free amino acids and free myo-inositol occur. These changes can be demonstrated by incubating a rabbit lens in a medium containing 30 mM. galactose. However, the lens incubated in galactose but also exposed to tetramethylene glutaric, an aldose reductase inhibitor, shows little dulcitol accumulation, a reduction in lens swelling, and preservation of the levels of free amino acids and myo-inositol at near normal levels. If the galactose-exposed lens is kept from swelling by media with appropriate tonicities, the levels of amino acids and inositol are also maintained near normal. The results suggest that depressed levels of these soluble components in the galactose-exposed lens may be due to osmotic effects caused by the retention of dulcitol. In the development of galactose cataract it appears that these early changes, along with electrolyte disturbances and equatorial opacities, are secondary to the primary event, which is the enzymatic reduction of galactose to dulcitol.

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