Abstract
Possible involvement of lipid peroxide (LPO) in the occurrence of diabetic retinal lesion was investigated using streptozotocin-induced diabetic rats. Young male Wistar rats weighing 100-150 g were made diabetic by daily i.p. injection of 30 mg/kg streptozotocin (STZ) for 5 days. Five weeks after the termination of STZ-treatment, when animals maintained typical hyperglycemia, the tissue level of LPO, estimated by the thiobarbituric acid method in the presence of 0.5 mM EDTA, was augmented in the kidney. At 7-9 wk after the STZ-treatment, the content of LPO in the retina also exhibited a significant increase, while those in the serum, brain and peripheral nerves showed no alteration. This increment of LPO in the kidney and retina was accompanied by the concomitant reduction of fat-soluble antioxidants determined by the ferric chloride-bipyridyl reaction, and insulin treatment (10 u/rat per day, s.c.) completely eliminated the increased formation of LPO in these organs. When diabetic rats were treated with retinol acetate, which had an inhibitory effect on LPO formation in retinal homogenate, the increase in LPO content was significantly suppressed, especially in the retina. The STZ-induced diabetic state may elicit an increased formation of LPO in the retina and kidney, both are main organs having typical diabetic lesions.