The absence of cataracts in mice with congenital hyperglycemia

Abstract

Investigations were conducted to determine the biochemical basis of the absence of cataracts in genetically diabetic mice. The resistance of these mice to cataracts appears to be due to the low activity of aldose reductase in the lens. Consequently only low amounts of polyols accumulate even after persistent hyperglycemia. The finding thus lends further support to the polyol theory of sugar cataractogenesis. The accumulation of sugar alcohols in galactosemic mice lenses was also much lower as compared to that in the lenses of galactosemic rats. A study was made of the enzymes that influence the polyol level in the lenses of various mouse strains. The activities of aldose reductase, polyol dehydrogenase, hexokinase and glucose-6-phosphate and 6-phosphogluconate dehydrogenases in the mouse and rat lenses were determined. The activities of all the enzymes except that of aldose reductase were similar in the lenses of both species. The aldose reductase activity in the mouse lens was only one tenth of that present in the rat lens.