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Part II

SIDNEY LERMAN, M.D.; Betty K. Ishida, B.S.

AMA Arch Ophthalmol. 1960;63(1):132-135.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

The cataractogenic influence of galactose is probably due to the fact that galactose-1-phosphate (Gal-1-P) acts as or gives rise to an inhibitor of glucose metabolism in the lens. This ester has been shown to accumulate to a tenfold excess in the lens capsule and lens epithelium of rats maintained on a high galactose diet.¹ Furthermore, a marked inhibition of the enzyme glucose-6-phosphate dehydrogenase (G-6-P) rapidly develops in the lenses of such animals, and a similar inhibition can be reproduced in vitro.^2,3 Four to six days following this enzyme inhibition, there is an apparent cessation of soluble protein synthesis.³ Although these observations indicate the locus where Gal-1-P might exert its cataractogenic influence, there are several other loci whereby this ester could possibly exert its deleterious effect. It might interfere with the initial phosphorylation of glucose to glucose-6-phosphate (the hexokinase reaction) as has been suggested by several investigators,^4,5 . . . [Full Text PDF of this Article]

Author Affiliations
Rochester, N.Y.

From the Department of Surgery, Division of Ophthalmology of the University of Rochester, School of Medicine and Dentistry.

Footnotes
Submitted for publication Aug. 10, 1959.

This investigation was supported by research funds granted by the Rochester Eye Bank and Research Society.

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