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Zinc enhances carnosine inhibitory effect against structural and functional age-related protein alterations in an albumin glycoxidation model
Biometals ( IF 4.1 ) Pub Date : 2020-09-30 , DOI: 10.1007/s10534-020-00254-0
Hichem Moulahoum 1 , Faezeh Ghorbanizamani 1 , Suna Timur 1, 2 , Figen Zihnioglu 1
Affiliation  

Age-related complications including protein alterations seen in diabetes and Alzheimer’s disease are a major issue due to their accumulation and deleterious effects. This report aims to investigate the effect of zinc supplementation on the anti-glycoxidation activity of carnosine on the in vitro model of albumin-based protein modification. Besides, the therapeutic effect of this combination was tested through the addition of the molecules in tandem (co-treatment) or post initiation (post-treatment) of the protein modification process. Glycation was induced via the addition of glucose to which carnosine (5 mM) alone or with various zinc concentrations (125, 250, and 500 μM) were added either at 0 h or 24 h post-glycation induction. On the other hand, protein oxidation was induced using chloramine T (20 mM) and treated in the same way with carnosine and zinc. The different markers of glycation (advanced glycation end products (AGEs), dityrosine, and beta-sheet formation (aggregation)) and oxidation (AOPP, advanced oxidation protein products) were estimated via fluorescence and colorimetric assays. Zinc addition induced a significant enhancement of carnosine activity by reducing albumin modification that outperformed aminoguanidine both in the co- and post-treatment protocols. Zinc demonstrated a supplementary effect in combination with carnosine highlighting its potential in the protection against age-related protein modifications processes such as the ones found in diabetes.



中文翻译:

在白蛋白糖氧化模型中,锌增强肌肽对结构和功能年龄相关蛋白改变的抑制作用

与年龄相关的并发症,包括糖尿病和阿尔茨海默病中的蛋白质改变,由于它们的积累和有害影响,是一个主要问题。本报告旨在研究补锌对基于白蛋白的蛋白质修饰体外模型中肌肽抗糖氧化活性的影响。此外,通过在蛋白质修饰过程的串联(共处理)或启动后(后处理)添加分子来测试这种组合的治疗效果。通过添加葡萄糖来诱导糖化,在糖化诱导后 0 小时或 24 小时,向其中单独添加肌肽 (5 mM) 或与各种锌浓度 (125、250 和 500 μM) 一起添加。另一方面,使用氯胺 T (20 mM) 诱导蛋白质氧化,并用肌肽和锌以相同方式处理。通过荧光和比色测定估计糖基化(高级糖基化终产物 (AGE)、二酪氨酸和 β-折叠形成(聚集))和氧化(AOPP,高级氧化蛋白产物)的不同标志物。锌添加通过减少白蛋白修饰导致肌肽活性显着增强,白蛋白修饰在联合治疗和治疗后均优于氨基胍。锌与肌肽结合显示出补充作用,突出了其在防止与年龄相关的蛋白质修饰过程(例如糖尿病中发现的过程)中的潜力。和β-折叠形成(聚集))和氧化(AOPP,高级氧化蛋白质产物)通过荧光和比色测定进行估计。锌添加通过减少白蛋白修饰导致肌肽活性显着增强,白蛋白修饰在联合治疗和治疗后均优于氨基胍。锌与肌肽结合显示出补充作用,突出了其在防止与年龄相关的蛋白质修饰过程(例如糖尿病中发现的过程)中的潜力。和β-折叠形成(聚集))和氧化(AOPP,高级氧化蛋白质产物)通过荧光和比色测定进行估计。锌添加通过减少白蛋白修饰导致肌肽活性显着增强,白蛋白修饰在联合治疗和治疗后均优于氨基胍。锌与肌肽结合显示出补充作用,突出了其在防止与年龄相关的蛋白质修饰过程(例如糖尿病中发现的过程)中的潜力。

更新日期:2020-09-30
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