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
LERMAN S, ISHIDA BK. Pathogenetic Factors in Experimental Galactose CataractPart III. AMA Arch Ophthalmol. 1960;63(1):136–139. doi:10.1001/archopht.1960.00950020138021
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