Abstract
Folic acid is a necessary micronutrient for normal human growth and development. Benzo(a)pyrene (BaP) is a ubiquitously distributed environmental pollutant and its metabolite, benzo(a)pyrene-diol-epoxide, is known to exert a strong teratogenic and carcinogenic effect on the body's tissues and cells. The aim of this study was to investigate the mechanism by which folic acid can inhibit the toxic effects of BaP both in vivo and in vitro. We measured changes in 16HBE cell activity affected by the intervention of folic acid on BaP using the cell counting kit-8 assay and that of cell cycle distribution by flow cytometry. At the same time, we assessed the xeroderma pigmentosum group A, xeroderma pigmentosum group C, excision repair cross complementation group 1, cyclinD1, and CKD4 mRNAs, and their related protein expression both in mouse lung tissue and in 16HBE cells. In conclusion, the mechanisms by which this effect is mediated were not entirely elucidated by our study, possibly because folic acid antagonizes the toxic effects of BaP by upregulating the levels of excision repair cross complementation group 1, xeroderma pigmentosum group A, and xeroderma pigmentosum group C gene expression to improve the rate of DNA repair, in turn accelerating the speed of repair for DNA damage caused by BaP. Meanwhile, folic acid could restrain BaP-induced cyclinD1 protein expression, which could help cells return to their normal cell cycle.