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Polymorphonuclear leukocyte injury by methylglyoxal and hydrogen peroxide: a possible pathological role for enhanced oxidative stress in chronic kidney disease

机译:甲基乙二醛和过氧化氢对多形核白细胞的伤害:慢性肾脏疾病中氧化应激增强的可能病理作用

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摘要

Background. Accelerated burst of polymorphonuclear leukocytes (PMNs) may be involved in the primary pathology of enhanced oxidative stress in patients with chronic kidney disease (CKD); however, the precise mechanism remains unknown. Methylglyoxal (MGO), an α-oxoaldehyde reportedly elevated in CKD, could induce apoptosis in several cell lines, and generates radicals by the reaction with hydrogen peroxide (H2O2). Thus, we tested if a high MGO of uraemic milieu could play a role in PMN injury by interaction with H2O2.
机译:背景。多形核白细胞(PMNs)的加速爆发可能参与了慢性肾脏病(CKD)患者氧化应激增强的主要病理过程。但是,确切的机制仍然未知。甲基乙二醛(MGO)是一种据称在CKD中升高的α-氧醛,可诱导几种细胞系凋亡,并通过与过氧化氢(H 2 O 2 )。因此,我们测试了尿毒症环境的高MGO是否可以通过与H 2 O 2 的相互作用在PMN损伤中发挥作用。

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