Lymphocyte DNA damage and oxidative stress in patients with iron deficiency anemia

被引:59
作者
Aslan, Mehmet [1 ]
Horoz, Mehmet
Kocyigit, Abdurrahim
Ozgonul, Saadet
Celik, Hakim
Celik, Metin
Erel, Ozcan
机构
[1] Harran Univ, Sch Med, Dept Internal Med, Sanliurfa, Turkey
[2] Harran Univ, Sch Med, Dept Biochem, Sanliurfa, Turkey
[3] Guven Med Ctr, Internal Med Clin, Sanliurfa, Turkey
关键词
iron deficiency anemia; DNA damage; plasma total antioxidant capacity; comet assay;
D O I
10.1016/j.mrfmmm.2006.06.013
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
Oxidant stress has been shown to play an important role in the pathogenesis of iron deficiency anemia. The aim of this study was to investigate the association between lymphocyte DNA damage, total antioxidant capacity and the degree of anemia in patients with iron deficiency anemia. Twenty-two female with iron deficiency anemia and 22 healthy females were enrolled in the study. Peripheral DNA damage was assessed using alkaline comet assay and plasma total antioxidant capacity was determined using an automated measurement method. Lymphocyte DNA damage of patients with iron deficiency anemia was significantly higher than controls (p < 0.05), while total antioxidant capacity was significantly lower (p < 0.001). While there was a positive correlation between total antioxidant capacity and hemoglobin levels (r = 0.706,p < 0.001), both total antioxidant capacity and hemoglobin levels were negatively correlated with DNA damage (r = -0.330, p < 0.05 and r = -0.323, p < 0.05, respectively). In conclusion, both oxidative stress and DNA damage are increased in IDA patients. Increased oxidative stress seems as an important factor that inducing DNA damage in those IDA patients. The relationships of oxidative stress and DNA damage with the severity of anemia suggest that both oxidative stress and DNA damage may, in part, have a role in the pathogenesis of IDA. (c) 2006 Elsevier B.V. All rights reserved.
引用
收藏
页码:144 / 149
页数:6
相关论文
共 25 条
  • [1] Mechanisms of DNA oxidation
    Aust, AE
    Eveleigh, JF
    [J]. PROCEEDINGS OF THE SOCIETY FOR EXPERIMENTAL BIOLOGY AND MEDICINE, 1999, 222 (03): : 246 - 252
  • [2] Glutathione peroxidase 1 activity and cardiovascular events in patients with coronary artery disease
    Blankenberg, S
    Rupprecht, HJ
    Bickel, C
    Torzewski, M
    Hafner, G
    Tiret, L
    Smieja, M
    Cambien, F
    Meyer, J
    Lackner, KJ
    [J]. NEW ENGLAND JOURNAL OF MEDICINE, 2003, 349 (17) : 1605 - 1613
  • [3] Humic acid-mediated oxidative damages to human erythrocytes: A possible mechanism leading to anemia in Blackfoot disease
    Cheng, ML
    Ho, HY
    Chiu, DTY
    Lu, FJ
    [J]. FREE RADICAL BIOLOGY AND MEDICINE, 1999, 27 (3-4) : 470 - 477
  • [4] The comet assay: What can it really tell us?
    Collins, AR
    Dobson, VL
    Dusinska, M
    Kennedy, G
    Stetina, R
    [J]. MUTATION RESEARCH-FUNDAMENTAL AND MOLECULAR MECHANISMS OF MUTAGENESIS, 1997, 375 (02) : 183 - 193
  • [5] CORRONS JLV, 1995, EUR J HAEMATOL, V55, P327
  • [6] DeMaeyer E, 1985, World Health Stat Q, V38, P302
  • [7] A novel automated method to measure total antioxidant response against potent free radical reactions
    Erel, O
    [J]. CLINICAL BIOCHEMISTRY, 2004, 37 (02) : 112 - 119
  • [8] The use of the alkaline comet assay with lymphocytes in human biomonitoring studies
    Faust, F
    Kassie, F
    Knasmüller, S
    Boedecker, RH
    Mann, M
    Mersch-Sundermann, V
    [J]. MUTATION RESEARCH-REVIEWS IN MUTATION RESEARCH, 2004, 566 (03) : 209 - 229
  • [9] Garcia O, 2004, MUTAT RES, V556, P151
  • [10] FREE-RADICALS, ANTIOXIDANTS, AND HUMAN-DISEASE - CURIOSITY, CAUSE, OR CONSEQUENCE
    HALLIWELL, B
    [J]. LANCET, 1994, 344 (8924) : 721 - 724