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为了探讨过氧化损伤与糖尿病肾病肾功能损害的关系，本文采用放射免疫分析法（RIA）对43例非胰岛素依赖型糖尿病（NIDDM）患者及28例健康对照者血清中的超过氧化物歧化酶（SOD）水平进行了观察，并将其与尿β2-微球蛋白排泄率（β2-MG）、白蛋白排泄率（Alb）、TammHorsfall糖蛋白排泄率（THP）、总蛋白排泄率（TP）、血尿素氮（BUN）及肌酐（Cr）含量之间的相互关系进行了分析。结果发现：MDDM患者中，不伴肾功能损害者，其SOD水平与健康成人比较无显著性差异（P＞0．05），而伴肾功能损害者，其SOD水平则明显低于健康成人（P＜0．01），且肾功能损害越重者，其SOD水平降低越明显。相关分析发现，伴肾功能损害者的SOD与TP呈显著负相关（n=27，r＝－0．39，P＜0．05）提示NIDDM患者体内SOD代谢失常，抗过氧化能力减弱，致肾小球遭受长期慢性的过氧化损伤可能是糖尿病肾病形成及发展机制中的中心环节。
In order to investigate the relationship between oxidative damage and renal function impairment in diabetic nephropathy, 43 patients with non-insulin dependent diabetes mellitus (NIDDM) and 28 healthy controls were assayed by radioimmunoassay (RIA) for serum levels of superoxide dismutase The levels of β2-MG, Alb, TammHorsfall glycoprotein excretion (THP), total protein excretion (TP) Blood urea nitrogen (BUN) and creatinine (Cr) content between the correlation analysis. The results showed that there was no significant difference in SOD level between MDDM patients and healthy adults (P> 0.05), while those with renal dysfunction were significantly lower than those in healthy adults P <0.01), and the heavier renal dysfunction, the more obvious the decrease of SOD level. Correlation analysis showed that there was a significant negative correlation between SOD and TP (n = 27, r = -0.39, P <0.05) in patients with renal dysfunction, suggesting abnormal SOD metabolism and decreased anti-peroxidation in patients with NIDDM Glomerular chronic long-term peroxidation damage may be the central link in the formation and development of diabetic nephropathy.