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Article
January 1960

Pathogenetic Factors in Experimental Galactose CataractPart II

Author Affiliations

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

AMA Arch Ophthalmol. 1960;63(1):132-135. doi:10.1001/archopht.1960.00950020134020
Abstract

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

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