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Article
March 1961

Pathogenetic Factors in Experimental Galactose CataractPart IV

Author Affiliations

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

Arch Ophthalmol. 1961;65(3):334-337. doi:10.1001/archopht.1961.01840020336004
Abstract

Previous communications have reported on certain biochemical changes that occur in the lenses of young rats (aged 28-32 days) maintained on a cataractogenic galactose diet.1-3 The accumulation of galactose-1-phosphate in these lenses apparently acts as or gives rise to an inhibitor of the enzyme glucose-6-phosphate dehydrogenase (G-6-P-D) during the first few days that these animals are maintained on a high galactose diet.1 The hexose monophosphate shunt is concurrently impaired as evidenced by a marked fall in the C1/C6 ratio of C14O2 recovered from these lenses incubated with glucose labeled in the number 1 or number 6 carbon atom.2 The concentration of high energy phosphate (ATP) in these lenses also decreases after the animals have been maintained on the diet for 3 days.

In order to further elucidate some of these changes that occur within the lens under the cataractogenic influence of

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