Dietary Intake of Proteins and Calories Is Inversely Associated With The Oxidation State of Plasma Thiols in End-Stage Renal Disease Patients.
Dietary Intake of Proteins and Calories Is Inversely Associated With The Oxidation State of Plasma Thiols in End-Stage Renal Disease Patients.
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DOI：
10.1053/j.jrn.2015.06.003
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发表时间：
2015-11
期刊：
影响因子：
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通讯作者：
Bansal S
中科院分区：
文献类型：
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作者：
Fanti P;Giustarini D;Rossi R;Cunningham SE;Folli F;Khazim K;Cornell J;Matteucci E;Bansal S
氧化应激导致维持性血液透析（MHD）患者蛋白质能量浪费（PEW）的发病机制。然而，食物摄入是否以及如何参与氧化应激与光能波之间的因果关系仍不确定。对 71 名成人 MHD 患者和 24 名健康受试者（对照）进行了横断面研究，分析饮食记录和氧化应激，通过一组血浆硫醇进行测量，包括蛋白质硫氢基 (-SH) 基团水平（PSH，总蛋白 -SH 还原能力的标志）、蛋白质硫醇化指数（PTI，二硫键，即蛋白质中氧化和还原 -SH 基团之间的比率）、低分子量 (LMM) 硫醇、LMM二硫化物和混合LMM-蛋白质二硫化物。此外，还测量了白细胞介素 6 (IL-6)、白蛋白、C 反应蛋白 (CRP) 和中性粒细胞明胶酶相关脂质运载蛋白 (NGAL) 作为炎症标志物。患者表现出低能量（22.0±8.4 Kcal/kg/d）和足够的蛋白质（1.0±0.4 g/kg/d）摄入量，高水平的胱氨酸[CySS；患者与对照：113.5 (90.9-132.8) vs. 68.2 (56.2-75.7) μM]，半胱氨酸化蛋白 [CySSP； 216.0 (182.8-254.0) vs. 163.5 (150.0-195.5) μM] 和高 PTI [0.76 (0.61 – 0.88) vs. 0.43 (0.40 – 0.54)；所有比较中 p<0.001]。在患者中，CySSP 的变化可以通过标准回归模型（R=0.775；p=0.00001）来解释，其中包括蛋白质摄入量（β=-0.361）、NGAL（β=0.387）、年龄（β=0.295）和白蛋白（β=0.457）的显着贡献。在同一模型中，PTI 的变化（R=0.624；p=0.01）可以通过蛋白质摄入量（β=-0.384）、年龄（β=0.326）和 NGAL（β=0.311）来解释。然而，当 PSH 作为因变量输入时（R=0.730；p=0.0001），只有血清白蛋白（β=0.495）和年龄（β=-0.280）对模型有贡献，而饮食摄入量或 NGAL 则对模型没有贡献。在 MHD 中，硫醇氧化标记物（包括 CySSP 和 PTI）显示与饮食摄入量和 NGAL 独立相关，而硫醇还原能力标记物 PSH 与这些相同的变量无关。 MHD 中氧化应激与食物摄入之间负相关的机制仍不清楚。
Oxidative stress contributes to the pathogenesis of protein-energy wasting (PEW) in maintenance hemodialysis (MHD) patients. It remains uncertain, however, whether and how food intake is involved in the causal relationship between oxidative stress and PEW. 71 adult MHD Patients and 24 healthy subjects (Control) were studied cross-sectionally with analyses of diet record and of oxidative stress, as measured by a battery of plasma thiols including the protein sulfhydryl (-SH) group levels (PSH, a marker of total protein –SH reducing capacity), the protein thiolation index (PTI, the ratio between disulfide, i.e. oxidized, and reduced –SH groups in proteins), low molecular mass (LMM) thiols, LMM disulfides and mixed LMM-protein disulfides. In addition, interleukin-6 (IL-6), albumin, C-reactive protein (CRP) and neutrophil gelatinase-associated lipocalin (NGAL) were measured as markers of inflammation. The Patients showed low energy (22.0±8.4 Kcal/kg/d) and adequate protein (1.0±0.4 g/kg/d) intakes, high levels of cystine [CySS; Patients vs. Control: 113.5 (90.9-132.8) vs. 68.2 (56.2-75.7) μM], cysteinylated proteins [CySSP; 216.0 (182.8-254.0) vs. 163.5 (150.0-195.5) μM] and high PTI [0.76 (0.61 – 0.88) vs. 0.43 (0.40 – 0.54); p<0.001 in all comparisons]. In Patients, variation of CySSP was explained by a standard regression model (R=0.775; p=0.00001) that included significant contributions of protein intake (β=−0.361), NGAL (β=0.387), age (β=0.295) and albumin (β=0.457). In the same model, variation of PTI (R=0.624; p=0.01) was explained by protein intake (β=−0.384) and age (β=0.326) and NGAL (β=0.311). However, when PSH was entered as dependent variable (R=0.730; p=0.0001) only serum albumin (β=0.495) and age (β=−0.280), but not dietary intake or NGAL, contributed to the model. In MHD, markers of thiol oxidation including CySSP and PTI show independent association with dietary intake and NGAL, while PSH, a marker of thiol reducing capacity, did not associate with these same variables. The mechanism(s) responsible for inverse association between oxidative stress and food intake in MHD remain undefined.