El-Far Mohamed A, Bakr Mohamed A, Farahat Sami E, Abd El-Fattah Elsaid A
Division of Biochemistry, Chemistry Department, Faculty of Science, Mansoura University, Mansoura, Egypt.
Clin Exp Nephrol. 2005 Jun;9(2):127-31. doi: 10.1007/s10157-005-0343-1.
Glutathione peroxidase (GPx) protects cells from oxidative damage by catalyzing the reduction of both organic and hydrogen peroxides, using glutathione as a reducing agent. Both plasma GPx (P-GPx) and erythrocyte GPx (E-GPx) have been identified in human blood. Kidney proximal tubular cells are the main source of GPx activity in the plasma. Oxidative damage has been reported to participate in the progression and complications of renal diseases.
The activities of both E-GPx and P-GPx were determined, using Randox commercial kits, in 12 patients with nephrotic syndrome (NS), 48 patients with renal impairment (RI), and 50 patients with chronic renal failure on maintenance hemodialysis (HD; before as well as immediately after dialysis), and in 50 healthy volunteers who served as controls.
Compared to the results in healthy controls, P-GPx activity was reduced in the HD group and the RI group, whereas the NS group showed no significant difference from the control. The HD group showed a higher drop in P-GPx (reduced to 36.6% of the mean control value) than the RI group (reduced to 61.8% of the mean control value). Further analysis of the RI group showed a highly significant negative correlation between P-GPx activity and serum creatinine level (r = -0.691; P < 0.001). Also, a highly significant negative correlation was found between P-GPx and blood urea nitrogen (r = -0.792; P < 0.001). However, E-GPx activity showed no significant correlation with either serum creatinine or blood urea nitrogen. E-GPx was reduced to 55.2% and 68.9% of the mean control 1 value in the NS group and the RI group respectively, while the HD group showed no significant change. Further analysis of the RI group found that E-GPx activity showed no significant correlation with either serum creatinine or blood urea nitrogen. In HD patients, GPx activity was measured before and immediately after hemodialysis. E-GPx activity was similar before and after dialysis, without a significant difference (pre-dialysis, 37.7 +/- 13.5 U/g hemoglobin [Hb]; post-dialysis, 38.72 +/- 12.31 U/g Hb). However, P-GPx activity was significantly increased (pre-dialysis, 254.4 +/- 62.6 U/ml; post-dialysis, 296.98 +/- 74.04 U/ml; P < 0.001), but it was still significantly lower when compared to that in the healthy controls.
P-GPx activity is an important test to assess the oxidative damage in patients with kidney diseases. The progression of renal disorders is accompanied by a decrease in P-GPx activity, but not by a decrease in E-GPx activity. Thus, we conclude that P-GPx activity largely depends on physiological renal function, whereas E-GPx activity does not.
谷胱甘肽过氧化物酶（GPx）通过以谷胱甘肽作为还原剂催化有机过氧化物和过氧化氢的还原反应，保护细胞免受氧化损伤。在人体血液中已鉴定出血浆GPx（P-GPx）和红细胞GPx（E-GPx）。肾近端小管细胞是血浆中GPx活性的主要来源。据报道，氧化损伤参与肾脏疾病的进展和并发症。
使用朗道（Randox）商用试剂盒测定了12例肾病综合征（NS）患者、48例肾功能损害（RI）患者和50例维持性血液透析（HD；透析前及透析后即刻）的慢性肾衰竭患者以及50名健康志愿者（作为对照）的E-GPx和P-GPx活性。
与健康对照组相比，HD组和RI组的P-GPx活性降低，而NS组与对照组无显著差异。HD组P-GPx活性下降幅度（降至平均对照值的36.6%）高于RI组（降至平均对照值的61.8%）。对RI组的进一步分析显示，P-GPx活性与血清肌酐水平呈高度显著负相关（r = -0.691；P < 0.001）。此外，P-GPx与血尿素氮之间也存在高度显著负相关（r = -0.792；P < 0.001）。然而，E-GPx活性与血清肌酐或血尿素氮均无显著相关性。NS组和RI组的E-GPx活性分别降至平均对照值的55.2%和68.9%，而HD组无显著变化。对RI组的进一步分析发现，E-GPx活性与血清肌酐或血尿素氮均无显著相关性。在HD患者中，于血液透析前及透析后即刻测定GPx活性。透析前后E-GPx活性相似，无显著差异（透析前，37.7±13.5 U/g血红蛋白[Hb]；透析后，38.72±12.31 U/g Hb）。然而，P-GPx活性显著升高（透析前，254.4±62.6 U/ml；透析后，296.98±74.04 U/ml；P < 0.001），但与健康对照组相比仍显著降低。
P-GPx活性是评估肾脏疾病患者氧化损伤的一项重要检测指标。肾脏疾病的进展伴随着P-GPx活性的降低，但E-GPx活性并未降低。因此，我们得出结论，P-GPx活性在很大程度上依赖于肾脏的生理功能，而E-GPx活性则不然。
