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Article
January 1960

Pathogenetic Factors in Experimental Galactose CataractPart III

AMA Arch Ophthalmol. 1960;63(1):136-139. doi:10.1001/archopht.1960.00950020138021
Abstract

The cataractogenic action of galactose is apparently due to a marked inhibition in the direct oxidative pathway of glucose-6-phosphate metabolism.1 The accumulation of galactose-1-phosphate in the lenses of animals maintained on a galactose diet2 acts as or gives rise to a specific inhibition of the enzyme glucose-6-phosphate dehydrogenase (G-6-P dehydrogenase).3 Since this enzyme is responsible for the first step in the direct oxidation of glucose-6-phosphate (G-6-P) to 6-phosphogluconate (6-P-G), an inhibition at this locus results in a marked depression of the hexose monophosphate shunt. In the experimental rat lens this inhibition occurs after the animal has been fed a 70% galactose diet for two and one-half to three days.1,3 Three to four days later, the synthesis of soluble lens proteins apparently ceases1,4; lens vacuoles first become manifest after 9-10 days on this diet, and a dense cataract develops in 12-18 days.

Since a sufficient supply

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