Hypochlorous acid generates Nε-(carboxymethyl) lysine from Amadori products
Hypochlorous acid generates Nε-(carboxymethyl) lysine from Amadori products
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DOI：
10.1080/10715760701332425
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发表时间：
2007-01-01
影响因子：
3.3
通讯作者：
Otagiri, Masaki
中科院分区：
文献类型：
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作者：
Mera, Katsumi;Nagai, Ryoji;Otagiri, Masaki
由于N-epsilon-(羧甲基)赖氨酸(CML)是一种主要的抗原性晚期糖基化终末产物，与高血糖和炎症的组织紊乱有关，因此CML形成途径的确定将为开发潜在的治疗这些并发症的策略提供重要信息。本研究旨在测定次氯酸(HOC1)对Amadori产品CML形成的影响。糖化人血清白蛋白(Glycated HSA)是Amadori产物的模型，与HOC1孵育可导致慢性粒细胞白血病的形成，HOC1浓度增加，pH降低，这与这些产物在炎症病变中的形成类似。当糖化人血清白蛋白与活化的中性粒细胞孵育时，也观察到慢性粒细胞白血病的形成，并在HOC1清除剂的存在下完全被抑制。这些数据表明，HOC1介导的慢性粒细胞白血病的形成在炎症部位的慢性粒细胞白血病的形成和组织损伤中发挥了作用。
Since the accumulation of N-epsilon-(carboxymethyl) lysine (CML), a major antigenic advanced glycation end product, is implicated in tissue disorders in hyperglycemia and inflammation, the identification of the pathway of CML formation will provide important information regarding the development of potential therapeutic strategies for these complications. The present study was designed to measure the effect of hypochlorous acid (HOC1) on CML formation from Amadori products. The incubation of glycated human serum albumin (glycated-HSA), a model of Amadori products, with HOC1 led to CML formation, and an increasing HOC1 concentration and decreasing pH, which mimics the formation of these products in inflammatory lesions. CML formation was also observed when glycated-HSA was incubated with activated neutrophils, and was completely inhibited in the presence of an HOC1 scavenger. These data demonstrated that HOC1-mediated CML formation from Amadori products plays a role in CML formation and tissue damage at sites of inflammation.