Abstract
DNA strand breaks have been evaluated in alloxan-diabetic dogs and experimentally galactosemic dogs, both animal models known to develop a retinopathy similar to that in diabetic patients. Lymphocytes were used as the source of DNA, and the presence of strand breaks was detected by monitoring the rate of alkali-induced DNA unwinding. The rate of DNA unwinding from dogs diabetic or galactosemic for up to 4 years was not significantly different from normal. These findings lend no support to previous reports that DNA strand breaks increase in diabetes or hyperglycemia. Retinopathy apparently can develop in the absence of DNA strand breaks, at least as estimated from lymphocytes.
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