Galactose cataract was produced in riboflavin deficient and riboflavin supplemented rats by feeding a 68% galactose diet deficient or supplemented with riboflavin. Twenty-three or twenty-five-day-old rats were fed riboflavin deficient and riboflavin supplemented diet for 21 days before feeding high galactose diet. About 80% of riboflavin deficient rats develop mature cataracts in 16-18 days after feeding riboflavin deficient high (68%) galactose diet whereas about 10% of rats fed a riboflavin supplemented high galactose diet for the same period develop mature cataracts. Progress in the formation of cataracts was followed by measuring biochemical parameters such as GSH, total thiol, protein thiol, and the levels of glutathione reductase, glucose-6-P dehydrogenase, and 6-phosphogluconate dehydrogenase in the lens. The levels of glutathione reductase, glucose-6-phosphate dehydrogenase, and 6-phosphogluconate dehydrogenase were lower in the lenses of riboflavin deficient than in normal rats fed galactose but GSH, total thiol, and protein thiol were not appreciably different in riboflavin deficient and control animals. Riboflavin deficiency alone does not lead to cataract formation in rat lenses when the rats were fed a riboflavin deficient diet for 16 weeks. Attempts to correct the increased susceptibility of riboflavin deficient rats to galactose cataract by either topical application of riboflavin or by injecting riboflavin into the anterior chamber of the eye were not successful.
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