ArticleGenes and environment : the official journal of the Japanese Environmental Mutagen Society2026
Mechanistic investigation of flavonoid-mediated inhibition of N-methyl-N-nitrosourea-induced mutagenicity via noncovalent DNA binding.
Article in Genes and environment : the official journal of the Japanese Environmental Mutagen Society, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundPrevious research using the Ames assay showed that licoricidin (LCD) and isoliquiritigenin (ILTG) can block mutations caused by N-methyl-N-nitrosourea (MNU) in Salmonella typhimurium (S. typhimurium) TA1535. With the aim to clarify the antimutagenic mechanism of these flavonoids, we evaluated the noncovalent interactions of test compounds (LCD, ILTG, ethidium bromide (EtBr), or Hoechst 33258) with calf thymus DNA (ctDNA) using a UV-Vis spectrophotometer and quantified the DNA adducts formed when treated with a mixture of MNU and the test compounds. Additionally, we measured the half-life of MNU and the amount of each test compound remaining in the reaction mixture.
resultsThe spectral and thermodynamic parameters indicated considerable binding between flavonoids (LCD and ILTG) and DNA. Intercalative EtBr and the minor-groove binder Hoechst 33258 inhibited MNU-induced mutagenicity in S. typhimurium TA1535. O
conclusionsLCD and ILTG directly bind to DNA and suppress DNA adduct formation. However, interaction with DNA alone does not fully account for their antimutagenic activity, implying the involvement of other mechanisms.
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