Mimić-Oka Jasmina, Savić-Radojević A, Pljesa-Ercegovac M, Opacić M, Simić T, Dimković N, Simić D V
Institute of Biochemistry, Faculty of Medicine, University of Belgrade, Belgrade, Serbia and Montenegro.
Ren Fail. 2005;27(3):345-51. doi: 10.1081/jdi-56599.
Parenteral iron has been recommended for the treatment of iron deficiency in the majority of maintenance hemodialyzed (HD) patients. However, iron supplementation and consequent over saturation of transferrin and high iron levels, may aggravate oxidative stress already present in these patients. This study aimed to further clarify the role of repeated intravenous iron therapy as a supplementary cause of oxidative stress in HD patients. Markers of free radical activities (carbonyl reactive derivatives, CRD, thiol groups, SH, malondialdehyde, MDA) and antioxidant enzyme activities (superoxide dismutase, SOD and glutathione peroxidase, GPX) were determined in plasma and red blood cells (RBC) of 19 hemodialysis patients given a total iron dose of 625 mg (ferrogluconat, Ferrlecit, 62.5 mg). Blood samples were taken before the first and after the last dose of iron. Twenty apparently normal subjects served as healthy controls. Before iron treatment, HD patients exhibited increased concentrations of MDA and CRD in plasma and red blood cells, accompanied with impaired antioxidant capacity. All patients responded to iron therapy with a significant increase in their serum ferritin, serum iron, hemoglobin, and red blood cells levels. However, iron treatment resulted in enhanced oxidative stress in plasma of HD patients, since significant increase in plasma MDA and CRD concentrations, together with a decrease in nonprotein SH groups levels were detected. Supplementation with iron did not significantly influence plasma SOD and GPX activities, nor did any of the red blood cell parameters tested. Our data show that, despite improvement in hematological parameters, an increase in iron stores due to supplementation could also contribute to increased free radical production in HD patients.
对于大多数维持性血液透析（HD）患者，已推荐使用胃肠外铁剂治疗缺铁。然而，铁补充以及随之而来的转铁蛋白过度饱和和高铁水平，可能会加重这些患者已存在的氧化应激。本研究旨在进一步阐明反复静脉补铁作为HD患者氧化应激补充原因的作用。在19例接受总铁剂量625mg（葡萄糖酸铁，Ferrlecit，62.5mg）的血液透析患者的血浆和红细胞（RBC）中，测定自由基活性标志物（羰基反应衍生物，CRD；巯基，SH；丙二醛，MDA）和抗氧化酶活性（超氧化物歧化酶，SOD；谷胱甘肽过氧化物酶，GPX）。在首次补铁前和末次补铁后采集血样。20名表面正常的受试者作为健康对照。在补铁治疗前，HD患者血浆和红细胞中的MDA和CRD浓度升高，同时抗氧化能力受损。所有患者补铁治疗后血清铁蛋白、血清铁、血红蛋白和红细胞水平均显著升高。然而，补铁治疗导致HD患者血浆氧化应激增强，因为检测到血浆MDA和CRD浓度显著升高，同时非蛋白SH基团水平降低。补铁对血浆SOD和GPX活性没有显著影响，对所检测的任何红细胞参数也没有显著影响。我们的数据表明，尽管血液学参数有所改善，但补铁导致的铁储存增加也可能导致HD患者自由基产生增加。
