Please use this identifier to cite or link to this item: http://cmuir.cmu.ac.th/jspui/handle/6653943832/59352
Title: Accumulation of lipid peroxidation-derived DNA lesions in iron-overloaded thalassemic mouse livers: Comparison with levels in the lymphocytes of thalassemia patients
Authors: Mayura Meerang
Jagadeesan Nair
Pornpan Sirankapracha
Chonthida Thephinlap
Somdet Srichairatanakool
Khelifa Arab
Ruchaneekorn Kalpravidh
Jim Vadolas
Suthat Fucharoen
Helmut Bartsch
Keywords: Biochemistry, Genetics and Molecular Biology
Medicine
Issue Date: 15-Aug-2009
Abstract: 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. © 2009 UICC.
URI: https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=67650065532&origin=inward
http://cmuir.cmu.ac.th/jspui/handle/6653943832/59352
ISSN: 10970215
00207136
Appears in Collections:CMUL: Journal Articles

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