Abstract
In previous study, we have known the colcemid inhibit UV-irradiated cell growth. Further, we also find the colcemid hinder the gap filling of nucleotide excision repair (NER). However, how the colcemid hamper the gap filling, the mechanism is still unclear. In this study, we have demonstrated (I) the oxidative DNA damage delayed the gap filling of NER and inhibition of gap filling was also found with typical BER-inducing agents such as hydrogen peroxide, menadione,and methyl methanesulfonate (MMS). We propose that competitionmay occur between NER and BER, which results in delay of gap filling. (II) We also propose that the flavonoids of propolis serve as temporary carriers of electrons received from transition metal ions that are relayed to oxygen molecules to subsequently generate superoxide and H2O2 which can induce oxidative DNA damage. (III) Over expression PCNA can attune the inhibition of gap, this result shows PCNA plays an important role not only in NER but in base excision repair (BER). However, ligase I and Fen-1 did not produce similar effects.