Isler Mehmet, Delibas Namik, Guclu Muhittin, Gultekin Fatih, Sutcu Recep, Bahceci Mehmet, Kosar Ali
Department of Internal Medicine, Suleyman Demirel University School of Medicine, Isparta, Turkey.
Croat Med J. 2002 Feb;43(1):16-9.
To test whether the activities of erythrocyte superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) can be affected by oral iron (OI) treatment, parenteral iron (PI) treatment, and parenteral iron treatment with vitamin E supplementation (PIE) in iron deficiency anemia.
Twenty-eight patients with iron deficiency anemia and 18 healthy controls were included in the study. Anemic patients were systematically allocated into 3 treatment groups. The first group (n=8) received OI, the second group (n=10) PI, and the third group (n=10) PIE. SOD and GSH-Px activities were determined using commercial kits.
Before the treatment, SOD activity was significantly lower in anemic patients than in the control group (Kruskal-Wallis test, p<0.05). After the treatment, SOD activity significantly increased in all three patient groups and reached the values found in the control group (Wicoxon signed-rank test, p=0.017 for OI, p=0.047 for PI, and p=0.037 for PIE group). Before the treatment, GSH-Px activities in anemic patients were similar to that of control group (Kruskal-Wallis test, p>0.05). Although there was no significant decrease in GSH-Px activity after OI treatment, both PI and PIE treatments significantly decreased GSH-Px activity (Wilcoxon signed-ranks test, p=0.007 for PI and p=0.005 for PIE). PIE was more effective than PI treatment in maintaining GSH-PX activity.
Oral iron treatment improved the iron deficiency anemia and recovered antioxidant defense system by increasing SOD activity and maintaining GSH-Px activity at normal level. When parenteral iron treatment is inevitable, vitamin E supplementation together with PI treatment may be effective in partially restoring the antioxidant status in this type of anemia.
检测缺铁性贫血患者口服铁剂（OI）治疗、胃肠外铁剂（PI）治疗以及胃肠外铁剂联合维生素E补充剂（PIE）治疗是否会影响红细胞超氧化物歧化酶（SOD）和谷胱甘肽过氧化物酶（GSH-Px）的活性。
本研究纳入了28例缺铁性贫血患者和18例健康对照者。贫血患者被系统地分为3个治疗组。第一组（n = 8）接受OI治疗，第二组（n = 10）接受PI治疗，第三组（n = 10）接受PIE治疗。使用商用试剂盒测定SOD和GSH-Px活性。
治疗前，贫血患者的SOD活性显著低于对照组（Kruskal-Wallis检验，p < 0.05）。治疗后，所有三个患者组的SOD活性均显著增加，并达到了对照组的水平（Wicoxon符号秩检验，OI组p = 0.017，PI组p = 0.047，PIE组p = 0.037）。治疗前，贫血患者的GSH-Px活性与对照组相似（Kruskal-Wallis检验，p > 0.05）。虽然OI治疗后GSH-Px活性没有显著降低，但PI和PIE治疗均显著降低了GSH-Px活性（Wilcoxon符号秩检验，PI组p = 0.007，PIE组p = 0.005）。PIE在维持GSH-PX活性方面比PI治疗更有效。
口服铁剂治疗改善了缺铁性贫血，并通过增加SOD活性和将GSH-Px活性维持在正常水平来恢复抗氧化防御系统。当胃肠外铁剂治疗不可避免时，PI联合维生素E补充剂治疗可能有效地部分恢复此类贫血的抗氧化状态。
