It has been demonstrated that myricetin, depending on its concentration, displays different oxidizing effects on DNA. Polyphenols like myricetin are able to reduce (donate electrons to) Fe3+. Thus, this reaction yields a less oxidized (more reduced) form of the iron cation: Fe2+ and a less reduced (more oxidized) form of myricetin.[1] This allows myricetin to form a complex with oxygen and biochemically target the DNA molecule. At higher and higher concentrations of myricetin, the rate of DNA damage has been shown to decrease.[1] A current hypothesis for why this occurs can be attributed to myricetin’s ability to chelate iron (Fe) (myricetin ligand forms two or more coordinate bonds to iron). These in vitro studies cannot be correlated directly to human models and should not be extrapolated.

Myricetin also impacts the biochemical efficacy and binding ability of large intracelluar biomolecules. Myricetin has been shown to inhibit viral reverse transcriptase, cellular DNA polymerase, and cellular RNA polymerase.[1] Inhibition of cellular DNA polymerases could have dangerous effects on the cell’s ability to replicate its genome and its progression through the cell cycle. Inhibition of cellular RNA polymerase could have deleterious effects on the cell’s capacity to transcribe and translate DNA and RNA to produce vital proteins for the cell. Researchers have found that myricetin has the ability to interfere in the RNA polymerase pathway in two different ways. In E. coli myricetin competitively inhibited GTP substrate binding to RNA polymerase. In T7 bacteriophages myricetin competitively inhibited DNA template binding to RNA polymerase.[1]
[1] https://www.sciencedirect.com/science/article/pii/S0306362396004211?via%3Dihub