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Products similar to non-enzymatic glycation end products are known to arise from the interactions between proteins and lipid peroxides in vitro. In this study, we assessed the effect of vitamin E, which possibly modifies lipid peroxide, on advanced glycation end products or similar products in vivo by measuring the fluorescence and thermal rupture time of tail tendon collagen in streptozotocin-induced diabetic rats. The diabetic rats and non-diabetic rats were fed a vitamin E supplemented diet, and a control diet starting 3 days after the streptozotocin injection. After the 4-week treatment, the serum lipid peroxide levels expressed as thiobarbituric acid reactants in the diabetic rats on control diet (15.9 +/- 2.6 mumol/l[SEM]) were significantly (p less than 0.05) higher than in the non-diabetic rats (7.9 +/- 1.3 mumol/l on control diet and 3.3 +/- 0.4 mumol/l on supplemented diet), but the levels in the diabetic rats on supplemented diet (7.9 +/- 2.3 mumol/l) were reduced to the normal levels. No significant differences were found in serum glucose and glycated haemoglobin levels within the diabetic rats on control and supplemented diets. Both the fluorescence and thermal rupture time of collagen were significantly (p less than 0.05) increased in the diabetic rats on both diets compared with those in the corresponding non-diabetic rats. Although there was no significant difference in the collagen-linked fluorescence within the diabetic rats on control and supplemented diets, the thermal rupture time was significantly (p less than 0.01) shortened with supplemented diet (10.8 +/- 0.7 min on supplemented diet vs 15.0 +/- 0.7 min on control diet).(ABSTRACT TRUNCATED AT 250 WORDS)

Protective effect of vitamin E supplementation on increased thermal stability of collagen in diabetic rats