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Article Abstract
PM induces oxidative/antioxidant system imbalance and excessive release of reactive oxygen species (ROS) and produces toxic effects and irreversible damage to the genetic material including chromosomes and DNA. Biochanin A (BCA), an isoflavone with strong antioxidant activity, effectively intervenes against PM-induced oxidative damage. The X-ray repair cross-complementary protein 1 (XRCC1)/BER pathway involves DNA damage repair caused by oxidative stress. This paper aims to explore the mechanism of BCA alleviating oxidative DNA damage caused by PM by establishing the cell model based on CRISPR/Cas9 technology and combining it with mechanism pathway research. The results showed that PM exposure inhibited the expression of BER and NER pathway proteins and induced the overexpression of ERCC1. BCA showed an effective intervention in the toxicity of PM in normal cells, rather than knock-out cells. This laid a foundation for further exploring the key role of in PM-caused oxidative damage and the BER/DNA damage repair pathway.
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