摘要
细胞内抗氧化酶合成(IAP)缺陷已在成人糖尿病肾病中得以证实。为了评价在患有1型糖尿病和有微血管病早期征象的青少年中,口服维生素E对IAP的影响, 笔者研究了12例青少年患者(年龄在11-21岁;糖尿病病程10-18年)。其中8例有视网膜病(病情分别为病变4例,增殖前病变3例,增殖性病变1例),4例有持续的微白蛋白尿症,并且7例同时有以上2种病变存在。通过组织活检和Dulbecco改良的伊格尔培养基培养,获得皮肤的成纤维细胞。在补充复合维生素E(600 mg, 2次/d)前后3个月测量CuZn过氧化物歧化酶(SOD)、
Defective intracellular antioxidant enzyme production (IAP) - has been demonstrated in adults with diabetic nephropathy. To evaluate the effects on IAP of vitamin E administration in adolescents with type 1 diabetes and early signs of microangiopathy, 12 adolescents (aged 11 -21 y; diabetes duration 10-18) were studied. Eight had retinopathy [background (four), preproliferative (three), or proliferative (one) ], four had persistent microaltumin-uria, and seven had both. Skin fibroblasts were obtained by biopsies and cultured in Dulbecco's modified Eagle's medium. CuZn Superoxide dismutase (SOD), MnSOD, catalase (CAT), and glutathione-peroxidase (GPX) activity and mRNA expression were measured before and after 3 mo of synthetic vitamin E supplementation (600 mg twice daily); on both occasions, IAP was evaluated at different ex. vivo glucose concentrations (5 and 22 mM) . Ten adolescents with type 1 diabetes (aged 12 -20 y) without angiopathy and eight healthy volunteers (aged 15 -22 y) participated as control subjects. Vitamin E serum levels were measured throughout the study. In normal glucose concentrations, CuZnSOD, MnSOD, CAT, and GPX activity and mRNA expression were not different among the groups. In high glucose, CuZnSOD activity and mRNA increased similarly in all groups [angiopathies: 0. 96 ±0.30 U/mg protein; 9.9 ±3.2 mRNA/glyceralde-hyde-3-phosphate dehydrogenase) . CAT and GPX activity and mRNA did not increase in high glucose only in adolescents with angiopathy (0. 35 ± 0.09; 4. 2±0. 1 and 0. 52 ± 0. 14; 2. 4 ±0. 9, respectively) . MnSOD did not change in any group. Vitamin E supplementation had no effect on any enzymatic activity and mRNA in both normal and hyperglycemic conditions. Adolescents with early signs of diabetic angiopathy have defective IAP and activity, which are not modified by vitamin E.
