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An investigation of the relation between catalase C262T gene polymorphism and catalase enzyme activity in leukemia patients

Introduction Catalase (CAT), an antioxidant enzyme, catalyzes conversion of hydrogen peroxide to water and molecular oxygen, protecting cells against oxidative stress. The aim of this study was to investigate the possible association between CAT C262T polymorphism in the promoter region of the CAT g...

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Bibliographic Details
Published in:Archives of medical science 2021, Vol.17 (4), p.928-933
Main Authors: Eras, Nazan, Türkoz, Gozde, Tombak, Anil, Tiftik, Naci, Yalin, Serap, Berkoz, Mehmet, Erden, Sema, Akbas, Etem
Format: Article
Language:English
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Summary:Introduction Catalase (CAT), an antioxidant enzyme, catalyzes conversion of hydrogen peroxide to water and molecular oxygen, protecting cells against oxidative stress. The aim of this study was to investigate the possible association between CAT C262T polymorphism in the promoter region of the CAT gene and leukemia risk and to determine the relationship between CAT genotypes and CAT enzyme activities. Material and methods Genotypes of 102 cases and 112 healthy controls’ genotypes were determined by polymerase chain reaction-restriction fragment length polymorphism methods. Catalase activity was measured with the method of Aebi. Results The frequencies of the T allele among the cases and controls were 28.4% and 25.9%, respectively (p = 0.75). The frequencies of CC, CT, and TT among cases were 57.8%, 27.4%, and 14.7%, respectively, while in controls, the frequencies of CC, CT, and TT were 54.4%, 39.3%, and 6.3%, respectively, which were not significantly different. Although CAT enzyme activity was lower in leukemia patients with TT genotypes than in controls, this did not reach statistical significance (p = 0.37). Conclusions This is the first report showing that CAT C262T polymorphism is not a genetic predisposing factor for the risk of leukemia in the Turkish population. However, additional research is needed to confirm these findings.
ISSN:1734-1922
1896-9151
DOI:10.5114/aoms.2019.89692