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首页> 外文期刊>Biochimica et biophysica acta. Molecular basis of disease: BBA >Fructose-mediated damage to lens α-crystallin: prevention by pyruvate
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Fructose-mediated damage to lens α-crystallin: prevention by pyruvate

机译：果糖介导的对晶状体α-晶状体蛋白的损害：丙酮酸的预防

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Post-translational modifications in lens crystallins due to glycation and oxidation have been suggested to play a significant role in the development of cataracts associated with aging and diabetes. We have previously shown that α-keto acids, like pyruvate, can protect the lens against oxidation. We hypothesize that they can also prevent the glycation of proteins competitively by forming a Schiff base between their free keto groups and the free - NH_2 groups of protein as well as subsequently inhibit the oxidative conversion of the initial glycation product to advanced glycation end products (AGE). The purpose of this study was to investigate these possibilities using purified crystallins. The crystallins isolated from bovine lenses were incubated with fructose in the absence and presence of pyruvate. The post-incubation mixtures were analyzed for fructose binding to the crystallins, AGE formation, and the generation of high molecular weight (HMW) proteins. In parallel experiments, the keto acid was replaced by catalase, superoxide dismutase (SOD), or diethylene triaminepentaacetic acid (DTPA). This was done to ascertain oxidative mode of pyruvate effects. Interestingly, the glycation and consequent formation of AGE from α-crystallin was more pronounced than from β-, and γ-crystallins. The changes in the crystallins brought about by incubation with fructose were prevented by pyruvate. Catalase, SOD, and DTPA were also effective. The results suggest that pyruvate prevents against fructose-mediated changes by inhibiting the initial glycation reaction as well as the conversion of the initial glycated product to AGE. Hence it is effective in early as well as late phases of the reactions associated with the formation of HMW crystallin aggregates.
机译：已提出由于糖基化和氧化而引起的晶状体晶状体蛋白的翻译后修饰在与衰老和糖尿病相关的白内障的发生中起重要作用。先前我们已经证明，α-酮酸（如丙酮酸）可以保护镜片免受氧化。我们假设它们还可以通过在蛋白质的游离酮基和游离的NH_2基团之间形成席夫碱来竞争性地阻止蛋白质的糖基化，并随后抑制初始糖基化产物向高级糖基化终产物（AGE）的氧化转化。 ）。这项研究的目的是研究使用纯化的结晶蛋白的这些可能性。在不存在和存在丙酮酸的情况下，将从牛晶状体分离的结晶蛋白与果糖一起孵育。孵育后的混合物进行了果糖与结晶蛋白的结合，AGE的形成以及高分子量（HMW）蛋白的产生的分析。在平行实验中，用过氧化氢酶，超氧化物歧化酶（SOD）或二亚乙基三胺五乙酸（DTPA）代替了酮酸。这样做是为了确定丙酮酸作用的氧化方式。有趣的是，由α-结晶蛋白形成的糖基化和随后形成的AGE比从β-和γ结晶蛋白形成的更为明显。丙酮酸可防止果糖温育引起的结晶蛋白变化。过氧化氢酶，SOD和DTPA也有效。结果表明丙酮酸通过抑制初始糖基化反应以及将初始糖基化产物转化为AGE来防止果糖介导的变化。因此，在与HMW结晶蛋白聚集体形成有关的反应的早期和晚期都有效。

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