Diabetic and galactosaemic cataracts.
An increased prevalence of cataract is associated with diabetes. Biochemical studies of diabetic lenses have revealed a variety of metabolic abnormalities including changes in the levels of electrolytes, glutathione, nucleotides and sugars. Similar biochemical changes have also been observed in cataracts associated with galactosaemia, suggesting that these sugar cataracts have a common biochemical aetiology. The common biochemical factor found to initiate both types of sugar cataract is the formation of sugar alcohols (polyols) from either glucose or galactose by the enzyme aldose reductase (alditol: NADP+ 1-oxidoreductase, EC 1.1.1.21). Increased intracellular levels of these polar alcohols have a hyperosmotic effect which leads to lens fibre swelling, vacuole formation and subsequent opacification. The process of sugar cataract formation in animals can be prevented by inhibiting aldose reductase.
D000449:Aldehyde Reductase / Q000037:antagonists & inhibitors / Q000378:metabolism; D000818:Animals; D002386:Cataract / Q000209:etiology* / Q000378:metabolism; D048909:Diabetes Complications; D003920:Diabetes Mellitus / Q000378:metabolism; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism; D005690:Galactose / Q000378:metabolism; D005693:Galactosemias / Q000150:complications* / Q000378:metabolism; D005947:Glucose / Q000378:metabolism; D006801:Humans; D007093:Imidazoles / Q000494:pharmacology; D048289:Imidazolidines; D007424:Intracellular Fluid / Q000378:metabolism; D007908:Lens, Crystalline / Q000378:metabolism; D051379:Mice; D009995:Osmosis; D051381:Rats; D013402:Sugar Alcohols / Q000378:metabolism*
D007093:Imidazoles; D048289:Imidazolidines; D013402:Sugar Alcohols; D000449:Aldehyde Reductase; C026411:sorbinil; D005947:Glucose; D005690:Galactose