Oxidative DNA damage: Induction by fructose, in vitro, and its enhancement by hydrogen peroxide.

Kaoru Midorikawa, Kokoro Kobayashi, Shinya Kato, Shosuke Kawanishi, Hatasu Kobayashi, Shinji Oikawa, Mariko Murata

Journal: Mutation research. Genetic toxicology and environmental mutagenesis 2024;893():503719

PMID: 38272630

Abstract

Sucrose and high-fructose corn syrup comprise nearly equal amounts of glucose and fructose. With the use of high-fructose corn syrup in the food industry, consumption of fructose, which may be a tumor promoter, has increased dramatically. We examined fructose-induced oxidative DNA damage in the presence of Cu(II), with or without the addition of HO. With isolated DNA, fructose induced Cu(II)-mediated DNA damage, including formation of 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG), to a greater extent than did glucose, and HO enhanced the damage. In cultured human cells, 8-oxodG formation increased significantly following treatment with fructose and the HO-generating enzyme glucose oxidase. Fructose may play an important role in oxidative DNA damage, suggesting a possible mechanism for involvement of fructose in carcinogenesis.

Copyright © 2023 The Authors. Published by Elsevier B.V. All rights reserved.

Address: Department of Environmental and Molecular Medicine, Mie University Graduate School of Medicine, Edobashi 2-174, Tsu, Mie 514-8507, Japan; Faculty of Child Education, Suzuka University, 663-222, Koriyama, Suzuka, Mie 510-0298, Japan.; Department of Environmental and Molecular Medicine, Mie University Graduate School of Medicine, Edobashi 2-174, Tsu, Mie 514-8507, Japan.; Radioisotope Experimental Facility, Advanced Science Research Promotion Center, Mie University, Edobashi 2-174, Tsu, Mie 514-8507, Japan.; Faculty of Pharmaceutical Science, Suzuka University of Medical Science, 3500-3, Minamitamagaki, Suzuka, Mie 513-8670, Japan.; Department of Environmental and Molecular Medicine, Mie University Graduate School of Medicine, Edobashi 2-174, Tsu, Mie 514-8507, Japan. Electronic address: [email protected].

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