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血液透析患者红细胞中甲基乙二醛生成增加。

Enhanced methylglyoxal formation in the erythrocytes of hemodialyzed patients.

作者信息

Karg Eszter, Papp Ferenc, Tassi Noemi, Janáky Tamás, Wittmann Gyula, Túri Sándor

机构信息

Department of Pediatrics, University of Szeged, Szeged, Hungary.

出版信息

Metabolism. 2009 Jul;58(7):976-82. doi: 10.1016/j.metabol.2009.02.032.

Abstract

Methylglyoxal (MG) contributes significantly to the carbonyl stress in uremia; however, the reason for its increased concentration is not clear. Thus, the present study was aimed to investigate the formation and degradation of MG in the erythrocytes of hemodialyzed (HD) patients with end-stage renal disease. In 22 nondiabetic patients on long-term HD, erythrocyte MG and d-lactate levels, glyoxalase activities, and whole blood reduced glutathione content were determined. The data were compared with those from 22 healthy controls. Erythrocyte MG and d-lactate production were also investigated in vitro under normoglycemic (5 mmol/L) and hyperglycemic (50 mmol/L) conditions. The erythrocyte MG levels were elevated (P < .001) in the HD patients. The blood reduced glutathione content and glyoxalase I activity were similar to the control levels, but the glyoxalase II activity was significantly (P < .005) increased. In the normoglycemic in vitro model, production of both MG (P < .001) and d-lactate (P < .002) was significantly enhanced in the HD erythrocytes relative to the controls. During hyperglycemia, the MG formation and degradation rates were further increased (P < .001). The present study demonstrated an increased formation of MG in the erythrocytes of HD patients. This seemed to be related to a glucose metabolism disturbance of the cells. The degradation system of MG was also activated; still, it was not able to counteract the high rate of MG formation. The alterations and imbalance of these metabolic processes may contribute to the carbonyl overload and stress in the HD patients.

摘要

甲基乙二醛(MG)在尿毒症的羰基应激中起重要作用;然而,其浓度升高的原因尚不清楚。因此,本研究旨在调查终末期肾病血液透析(HD)患者红细胞中MG的形成和降解情况。对22例长期接受HD治疗的非糖尿病患者测定其红细胞MG和d-乳酸水平、乙二醛酶活性及全血还原型谷胱甘肽含量,并与22例健康对照者的数据进行比较。同时,在正常血糖(5 mmol/L)和高血糖(50 mmol/L)条件下体外研究红细胞MG和d-乳酸的产生情况。HD患者红细胞MG水平升高(P <.001)。血液还原型谷胱甘肽含量和乙二醛酶I活性与对照水平相似,但乙二醛酶II活性显著升高(P <.005)。在正常血糖体外模型中,HD患者红细胞中MG(P <.001)和d-乳酸(P <.002)的产生相对于对照组均显著增强。在高血糖期间,MG的形成和降解速率进一步增加(P <.001)。本研究表明HD患者红细胞中MG的形成增加,这似乎与细胞的葡萄糖代谢紊乱有关。MG的降解系统也被激活,但仍无法抵消MG的高形成速率。这些代谢过程的改变和失衡可能导致HD患者的羰基过载和应激。

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