Oxidative stress is implicated in the pathogenesis and complications of type 2 diabetes mellitus (NIDDM). Glycoxidation may damage the enzymes that synthesise glutathione (GSH), an endogenous intracellular antioxidant. Erythrocytes (RBCs) taken from NIDDM subjects, and non-diabetic controls, were GSH-depleted using 1-chloro-2,4-dinitrobenzene, incubated in a solution containing GSH-rebuilding substrates, and sampled for GSH using a 5,5'-gamma-dithiobis-(2-nitrobenzoic acid)/enzymatic recycling procedure. NIDDM subjects, on average, had the same GSH concentration and synthesising ability as non-diabetic controls, indicating normal function of the synthesis enzymes. A positive correlation between synthesis and concentration of GSH seen in non-diabetic controls did not exist in NIDDM, due to their putatively larger oxidative load. The results, to the best of our knowledge, provide the first evidence that, despite a higher oxidative load, intact RBCs from NIDDM subjects are able to synthesise GSH normally. It is hypothesised that increased rates of GSH synthesis would maintain a normal steady-state GSH concentration.

中文翻译：

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2型糖尿病患者的红细胞合成谷胱甘肽。

氧化应激与2型糖尿病（NIDDM）的发病机理和并发症有关。糖氧化可能破坏合成内源性细胞内抗氧化剂谷胱甘肽（GSH）的酶。取自NIDDM受试者和非糖尿病对照的红细胞（RBC），使用1-氯-2,4-二硝基苯对GSH进行耗竭，在含有GSH重建底物的溶液中孵育，并使用5,5'进行GSH采样-γ-二硫代双（2-硝基苯甲酸）/酶循环程序。NIDDM受试者平均具有与非糖尿病对照相同的GSH浓度和合成能力，表明合成酶的功能正常。NIDDM中不存在非糖尿病对照组中GSH的合成与浓度之间的正相关关系，因为它们的氧化负荷可能更大。结果，据我们所知，第一个证据表明，尽管氧化负荷较高，来自NIDDM受试者的完整RBC仍能够正常合成GSH。假设增加的GSH合成速率将维持正常的稳态GSH浓度。