类风湿、银屑病、幼年特发性关节炎和骨关节炎患者的血清硒、硒蛋白 P 和谷胱甘肽过氧化物酶 3。

IF 4.8 2区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Journal of Nutritional Biochemistry Pub Date : 2024-10-09 DOI:10.1016/j.jnutbio.2024.109776

Lukas Wahl , Thilo Samson Chillon , Petra Seemann , Sarah Ohrndorf , Ragna Ochwadt , Wolfgang Becker , Lutz Schomburg , Paula Hoff

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引用次数: 0

摘要

简介硒蛋白 P (SELENOP) 控制硒的运输，谷胱甘肽过氧化物酶 3 (GPx3) 在血液中激发抗氧化活性。炎症与硒缺乏有关，但有关炎症性风湿性肌肉骨骼疾病（iRMD）中硒蛋白的知识却很有限。我们比较了类风湿（RA）、银屑病（PsA）和幼年特发性关节炎（JIA）患者与骨关节炎（OA）和健康人的三种硒生物标志物，以完善 iRMD 中硒蛋白表达的数据基础：这项横断面研究共招募了272名RA（131人）、PsA（67人）、JIA（22人）和OA（52人）患者。血清中的硒通过全反射X射线荧光法进行定量，SELENOP通过酶联免疫吸附法进行定量，GPx3通过酶法测试进行定量。EPIC 试验的数据作为参考。日常生活障碍通过功能能力问卷（FfbH）进行评估：结果：在所有组别中，血清 SELENOP 和 Se 浓度呈线性相关，均低于 EPIC 试验中测得的平均值。不同患者组之间的硒浓度没有差异。与对照组相比，iRMD 患者的 SELENOP 水平较低。JIA和PsA患者的GPx3活性特别低。血清反应阳性的 RA 患者与血清反应阴性的 RA 患者之间的 GPx3 与 Se 或 SELENOP 之间的相互作用被破坏。SELENOP与FfbH测量的功能状态相关，在OA中最为明显（R=0.76，p讨论：数据表明，大多数 iRMD 患者缺乏硒蛋白，而 SELENOP 与 OA 的功能状态呈正相关。由于增加 Se 的供应可改善硒蛋白的生物合成，因此值得考虑对诊断出的缺乏症进行个性化矫正，以改善 Se 的转运并减轻疾病负担。

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Serum selenium, selenoprotein P and glutathione peroxidase 3 in rheumatoid, psoriatic, juvenile idiopathic arthritis, and osteoarthritis

Selenoprotein P (SELENOP) controls selenium (Se) transport, and glutathione peroxidase 3 (GPx3) elicits antioxidant activity in blood. Inflammation associates with Se deficiency, but knowledge concerning selenoproteins in inflammatory rheumatic musculoskeletal diseases (iRMD) is limited. We compared three Se biomarkers in patients with rheumatoid (RA), psoriatic (PsA), and juvenile idiopathic arthritis (JIA) in comparison to osteoarthritis (OA) and healthy subjects, to improve the data base on selenoprotein expression in iRMD.

The cross-sectional study enrolled n=272 patients with RA (n=131), PsA (n=67), JIA (n=22) and OA (n=52). Serum Se was quantified by total reflection X-ray fluorescence, SELENOP by ELISA and GPx3 by an enzymatic test. Data from the EPIC trial served as reference. Impairment of daily life was assessed by the Functional Ability Questionnaire (FfbH).

Serum SELENOP and Se concentrations correlated linearly in all groups and were below the average measured in EPIC. Se concentration was not different between the patient groups. Compared to controls, SELENOP levels were low in iRMD patients. GPx3 activity was particularly low in JIA and PsA. Seropositive but not seronegative RA patients displayed a disrupted interaction between GPx3 and Se or SELENOP. SELENOP associated with the functional status measured by the FfbH, most pronounced in OA (R=0.76, P < .01).

The data indicate selenoprotein deficiency in the majority of patients with iRMD, and a positive relation of SELENOP with functional status in OA. Since increased Se supply improves selenoprotein biosynthesis, a personalized correction of diagnosed deficiency merits consideration to improve Se transport and ameliorate disease burden.

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来源期刊

Journal of Nutritional Biochemistry 医学-生化与分子生物学

CiteScore

9.50

自引率

3.60%

发文量

237

审稿时长

68 days

期刊介绍： Devoted to advancements in nutritional sciences, The Journal of Nutritional Biochemistry presents experimental nutrition research as it relates to: biochemistry, molecular biology, toxicology, or physiology. Rigorous reviews by an international editorial board of distinguished scientists ensure publication of the most current and key research being conducted in nutrition at the cellular, animal and human level. In addition to its monthly features of critical reviews and research articles, The Journal of Nutritional Biochemistry also periodically publishes emerging issues, experimental methods, and other types of articles.