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首页> 外文期刊>Kidney international. >Increased plasma protein homocysteinylation in hemodialysis patients
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Increased plasma protein homocysteinylation in hemodialysis patients

机译：血液透析患者血浆蛋白同型半胱氨酸增加

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Hyperhomocysteinemia, an independent cardiovascular risk factor, is present in the majority of hemodialysis patients. Among the postulated mechanisms of toxicity, protein homocysteinylation is potentially able to cause significant alterations in protein function. Protein homocysteinylation occurs through various mechanisms, among which is the post-translational acylation of free amino groups (protein-N-homocysteinylation, mediated by homocysteine (Hcy) thiolactone). Another type of protein homocysteinylation occurs through the formation of a covalent -S-S- bond, found primarily with cysteine residues (protein-S-homocysteinylation). Scant data are available in the literature regarding the extent to which alterations in protein homocysteinylation are present in uremic patients on hemodialysis, and the effects of folate treatment are not known. Protein homocysteinylation was measured in a group of hemodialysis patients (n=28) compared to controls (n=14), with a new method combining protein reduction, gel filtration and Hcy derivatization. Chemical hydrolysis was performed, followed by high-pressure liquid chromatography separation. The effects of folate treatment on protein homocysteinylation, as well as in vitro binding characteristics were evaluated. Plasma Hcy, protein-N-homocysteinylation and protein-S-homocysteinylation were significantly higher in patients vs controls. Plasma Hcy and protein-S-homocysteinylation were significantly correlated. After 2 months of oral folate treatment, protein-N-homocysteinylation was normalized, and protein-S-homocysteinylation was significantly reduced. Studies on albumin-binding capacity after in vitro homocysteinylation show that homocysteinylated albumin is significantly altered at the diazepam-binding site. In conclusion, increased protein homocysteinylation is present in hemodialysis patients, with possible consequences in terms of protein function. This alteration can be partially reversed after folate treatment.
机译：高同型半胱氨酸血症是一种独立的心血管危险因素，存在于大多数血液透析患者中​​。在假定的毒性机制中，蛋白质高半胱氨酸化可能会引起蛋白质功能的重大改变。蛋白质高半胱氨酸化通过多种机制发生，其中包括游离氨基的翻译后酰化（蛋白质-N-高半胱氨酸化，由高半胱氨酸（Hcy）硫代内酯介导）。蛋白质同型半胱氨酸化的另一种类型是通过形成共价-S-S-键而发生的，主要通过半胱氨酸残基发现（蛋白-S-同型半胱氨酸化）。关于尿毒症患者血液透析中蛋白质同型半胱氨酸化程度改变的程度，文献中尚无相关数据，但叶酸治疗的作用尚不清楚。与对照组（n = 14）相比，一组血液透析患者（n = 28）进行了蛋白质同型半胱氨酸化检测，采用了一种结合蛋白质还原，凝胶过滤和Hcy衍生化的新方法。进行化学水解，然后进行高压液相色谱分离。评估了叶酸处理对蛋白质同型半胱氨酸化的影响以及体外结合特性。与对照组相比，患者血浆Hcy，蛋白质-N-半胱氨酸化和蛋白质-S-半胱氨酸化显着更高。血浆Hcy和蛋白质-S-同型半胱氨酸化显着相关。口服叶酸治疗2个月后，蛋白N-高半胱氨酸化水平正常化，蛋白S-高半胱氨酸化程度明显降低。体外高半胱氨酸化后白蛋白结合能力的研究表明，高半胱氨酸化的白蛋白在地西epa结合位点显着改变。总之，血液透析患者存在较高的蛋白质同型半胱氨酸化作用，可能会对蛋白质功能造成影响。叶酸治疗后，这种改变可以部分逆转。

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