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Japanese Journal of Cancer Research : Gann logoLink to Japanese Journal of Cancer Research : Gann
. 2002 Mar;93(3):247–252. doi: 10.1111/j.1349-7006.2002.tb02165.x

Lack of Direct Involvement of 8‐Hydroxy‐2′‐deoxyguanosine in Hypoxanthine‐guanine Phosphoribosyltransferase Mutagenesis in V79 Cells Treated with N,N'‐Bis(2‐hydroxyperoxy‐2‐methoxyethyl)‐l,4,5,8‐naphthalenetetracarboxylic‐diimide (NP‐III) or Riboflavin

Madoka Nakajima 1, Toru Takeuchi 2, Keiki Ogino 1, Kanehisa Morimoto 3,
PMCID: PMC5926961  PMID: 11927005

Abstract

The object of this study is to investigate the relationship between a typical product of oxidative DNA damage, 8‐hydroxy‐2′‐deoxyguanosine (8OHdG), and mutagenesis in V79 cells through a molecular analysis of hypoxanthine‐guanine phosphoribosyltransferase (hprt) gene mutants. We performed a direct sequencing analysis of the cDNA of mutants obtained after treatment with N,N'‐bis(2‐hydroxyperoxy‐2‐methoxyethyl)‐l,4,5,8‐naphthalenetetracarboxylic‐diimide (NP‐III) or riboflavin, each of which induces the formation of 8OHdG in cellular DNA upon UVA irradiation. The frequency of mutation after both treatments was no more than 2 to 5 times the control value. A considerable number of the mutants could not be amplified by RT‐PCR, and this was also the case for the control mutants. Among the mutants analyzed, deletions and a TA→Ã transversion occurred predominantly. The reasons for the weak association of induction of 8OHdG with frequency of mutation and the possible mechanism of oxidative‐stress‐derived mutagenesis are discussed.

Keywords: 8‐Hydroxy‐2′‐deoxyguanosine, hprt, Mutation, Deletion

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