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Dysregulation of Superoxide Dismutase in Chronic Sidney Disease

机译:慢性悉尼病中超氧化物歧化酶的异常调节

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Chronic kidney disease (CKD) is commonly reported to be associated with oxidative stress but there is still controversy on the mechanism. Numerous sources of radical oxygen species (ROS) have been identified in CKD patients, especially in hemodialysis (HD) patients. Macro-phage activation, which produces ROS, is due in these patients to: accumulation of uremic toxins; dialysis membrane bio-incompatibility; influx of endotoxins from the dialysate, and immunologic and metabolic disorders such as diabetes and dyslipidemia [1]. Phagocyte myeloper-oxidase-mediated events have also been associated with the production of oxidized low-density lipoprotein [2]; advanced oxidation protein products and advanced gly-cation end products, which are considered potent mediators of inflammation [3]. Moreover, treatment of anemia with high levels of iron may induce oxidative stress [4]. The massive generation of ROS is all the more damaging given that CKD patients have a weaker antioxidant system due to a diet low in antioxidant vitamins and oligo-elements [5] and due to loss of antioxidants during HD sessions [6].
机译:慢性肾病(CKD)通常被报道与氧化应激有关,但其机理尚有争议。在CKD患者中,尤其是在血液透析(HD)患者中,已经鉴定出多种自由基氧(ROS)来源。在这些患者中,产生ROS的巨噬细胞活化是由于:尿毒症毒素的积累;透析膜生物不相容性;内毒素从透析液中流入,以及免疫和代谢疾病,例如糖尿病和血脂异常[1]。吞噬细胞髓过氧化物酶介导的事件也与氧化的低密度脂蛋白的产生有关[2]。先进的氧化蛋白产物和先进的糖基阳离子终产物,它们被认为是炎症的有效介体[3]。此外,用高铁水平治疗贫血可能会引起氧化应激[4]。鉴于CKD患者的抗氧化剂系统较弱,这是由于饮食中抗氧化剂维生素和寡元素含量较低[5]以及HD期间抗氧化剂的流失[6]所致,因此大量ROS更具破坏性。

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