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March 1961

Pathogenetic Factors in Experimental Galactose Cataract: Part 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

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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