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黄嘌呤氧化酶在血液透析诱导的氧化损伤中的作用:与营养状况的关系。

The role of xanthine oxidase in hemodialysis-induced oxidative injury: relationship with nutritional status.

机构信息

Institute of Biochemistry, Medical Faculty Pristina, 38220 Kosovska Mitrovica, Serbia.

出版信息

Oxid Med Cell Longev. 2013;2013:245253. doi: 10.1155/2013/245253. Epub 2013 Jun 2.

Abstract

The role of xanthine oxidase (XOD) in patients undergoing chronic hemodialysis treatment (HD) is poorly understood. Geriatric nutritional risk index (GNRI) ≤ 90 could be linked with malnutrition-inflammation complex syndrome. This study measured XOD, myeloperoxidase (MPO), superoxide dismutase (SOD), lipid hydroperoxides, total free thiol groups, and advanced oxidation protein products (AOPP) in 50 HD patients before commencing (pre-HD) and immediately after completion of HD session (post-HD) and in 22 healthy controls. Pre-HD serum hydroperoxides, AOPP, XOD, and SOD were higher and total thiol groups were lower in patients than in controls (P < 0.05, resp.). Compared to baseline values, serum MPO activity was increased irrespective of GNRI status. Serum XOD activity was increasing during HD treatment in the group with GNRI ≤ 90 (P = 0.030) whilst decreasing in the group with GNRI > 90 (P = 0.002). In a multiple regression analysis, post-HD serum XOD activity was independently associated with GNRI ≤ 90 ( β ± SE: 0.398 ± 0.151; P = 0.012) and HD vintage ( β ± SE: -0.349 ± 0.139; P = 0.016). These results indicate that an upregulated XOD may be implicated in HD-induced oxidative injury contributing to accelerated protein damage in patients with GNRI ≤ 90.

摘要

黄嘌呤氧化酶(XOD)在接受慢性血液透析治疗(HD)的患者中的作用知之甚少。老年营养风险指数(GNRI)≤90 可能与营养不良-炎症复合综合征有关。本研究在 50 名开始 HD 治疗前(pre-HD)和 HD 治疗结束后(post-HD)以及 22 名健康对照者中测量了 XOD、髓过氧化物酶(MPO)、超氧化物歧化酶(SOD)、脂质氢过氧化物、总游离巯基和晚期氧化蛋白产物(AOPP)。与对照组相比,HD 患者的 pre-HD 血清氢过氧化物、AOPP、XOD 和 SOD 较高,总巯基组较低(P<0.05,分别)。与基线值相比,无论 GNRI 状态如何,血清 MPO 活性均增加。在 GNRI≤90 的组中,血清 XOD 活性在 HD 治疗期间增加(P=0.030),而在 GNRI>90 的组中则降低(P=0.002)。在多元回归分析中,post-HD 血清 XOD 活性与 GNRI≤90 独立相关(β±SE:0.398±0.151;P=0.012)和 HD 复古(β±SE:-0.349±0.139;P=0.016)。这些结果表明,上调的 XOD 可能与 HD 诱导的氧化损伤有关,导致 GNRI≤90 的患者蛋白质损伤加速。

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