Accumulation of lipid peroxidation-derived DNA lesions in iron-overloaded thalassemic mouse livers: Comparison with levels in the lymphocytes of thalassemia patients

Mayura Meerang, Jagadeesan Nair, Pornpan Sirankapracha, Chonthida Thephinlap, Somdet Srichairatanakool, Khelifa Arab, Ruchaneekorn Kalpravidh, Jim Vadolas, Suthat Fucharoen, Helmut Bartsch

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21 Citations (Scopus)


In thalassemia patients, iron overload can stimulate lipid peroxidation (LPO), thereby generating miscoding DNA adducts. Adducted DNA was measured in the lymphocytes of β-Thal/Hb E patients and healthy controls and in the organs of thalassemic mice. εdA, εdC and M1dG residues were quantified by 32P-postlabeling-TLC/HPLC. M1dG levels in lymphocyte DNA from patients were 4 times as high as in controls, while the increase in εdA and εdC was not significant. Adducted DNA accumulated in the liver of thalassemic mice having >2.7 mg Fe/g tissue dry weight; DNA adducts and iron were highly correlated. edA was not specifically generated in certain mouse liver cell types as revealed by immunohistochemical staining. We found elevated LPO-induced DNA damage in the liver of thalassemic mouse and in lymphocytes, implicating that massive DNA damage occurs in the liver of thalassemia patients. We conclude that promutagenic LPO-derived DNA lesions are involved in the onset of hepatocellular carcinoma in these patients.

Original languageEnglish
Pages (from-to)759-766
Number of pages8
JournalInternational Journal of Cancer
Issue number4
Publication statusPublished - 15 Aug 2009
Externally publishedYes


  • Etheno-DNA adducts
  • Iron overload
  • Lipid peroxidation
  • Thalassemia

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