Pathogenetic Factors in Experimental Galactose Cataract

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