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首页> 外文期刊>Biochemical and Biophysical Research Communications >Methylglyoxal induces cellular damage by increasing argpyrimidine accumulation and oxidative DNA damage in human lens epithelial cells.
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Methylglyoxal induces cellular damage by increasing argpyrimidine accumulation and oxidative DNA damage in human lens epithelial cells.

机译：甲基乙二醛通过增加精氨酸嘧啶累积和人晶状体上皮细胞中的氧化DNA损伤来诱导细胞损伤。

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摘要

Methylglyoxal (MGO) is a cytotoxic metabolite and modifies tissue proteins through the Maillard reaction, resulting in advanced glycation end products (AGEs), which can alter protein structure and functions. Several MGO-derived AGEs have been described, including argpyrimidine, a fluorescent product of the MGO reaction with arginine residues. Herein, we evaluated the cytotoxic role of MGO in human lens epithelial cell line (HLE-B3). HLE-B3 cells were exposed to 400 microM MGO in the present or absence of pyridoxamine for 24h. We then examined the formation of argpyrimidine, apoptosis and oxidative stress in HLE-B3 cells. In MGO-treated HLE-B3 cells, the accumulation of argpyrimidine was markedly increased, and caspase-3 and 8-hydroxydeoxyguanosine (8-OHdG) were highly expressed, which paralleled apoptotic cell death. However, pyridoxamine (AGEs inhibitor) prevented the argpyrimidine formation and apoptosis of MGO-treated HLE-B3 cells. These results suggested that the accumulation of argpyrimidine and oxidative DNA damage caused by MGO are involved in apoptosis of HLE-B3 cells.
机译：甲基乙二醛（MGO）是一种具有细胞毒性的代谢产物，通过美拉德反应修饰组织蛋白，产生高级糖基化终产物（AGEs），可以改变蛋白质的结构和功能。已经描述了几种MGO衍生的AGE，包括argpyrimidine，这是MGO反应中带有精氨酸残基的荧光产物。本文中，我们评估了MGO在人晶状体上皮细胞系（HLE-B3）中的细胞毒作用。在存在或不存在吡ido胺的情况下，将HLE-B3细胞暴露于400 microM MGO中24小时。然后，我们检查了HLE-B3细胞中精氨酸嘧啶的形成，细胞凋亡和氧化应激。在经MGO处理的HLE-B3细胞中，argpyrimidine的积累显着增加，并且caspase-3和8-羟基脱氧鸟苷（8-OHdG）高度表达，与凋亡的细胞死亡平行。但是，吡ido胺（AGEs抑制剂）阻止了argpyrimidine的形成和MGO处理的HLE-B3细胞的凋亡。这些结果表明，精氨酸嘧啶的积累和由MGO引起的氧化性DNA损伤与HLE-B3细胞的凋亡有关。

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