Cadmium (Cd) is a widespread environmental pollutant and carcinogen. Although the\nexact mechanisms of Cd-induced carcinogenesis remain unclear, previous acute/chronic Cd exposure\nstudies have shown that Cd exerts its cytotoxic and carcinogenic effects through multiple mechanisms,\nincluding interference with the DNA repair system. However, the effects of post-chronic Cd exposure\nremain unknown. Here, we establish a unique post-chronic Cd-exposed human lung cell model\n(the â??CR0â? cells) and investigate the effects of post-chronic Cd exposure on the DNA repair system.\nWe found that the CR0 cells retained Cd-resistant property even though it was grown in Cd-free\nculture medium for over a year. The CR0 cells had lasting DNA damage due to reduced DNA\nrepair capacity and an aberrant DNA repair gene expression profile. A total of 12 DNA repair genes\nassociated with post-chronic Cd exposure were identified, and they could be potential biomarkers\nfor identifying post-chronic Cd exposure. Clinical database analysis suggests that some of the DNA\nrepair genes play a role in lung cancer patients with different smoking histories. Generally, CR0 cells\nwere more sensitive to chemotherapeutic (cisplatin, gemcitabine, and vinorelbine tartrate) and DNA\ndamaging (H2O2) agents, which may represent a double-edged sword for cancer prevention and\ntreatment. Overall, we demonstrated for the first time that the effects of post-chronic Cd exposure on\nhuman lung cells are long-lasting and different from that of acute and chronic exposures. Findings\nfrom our study unveiled a new perspective on Cd-induced carcinogenesis--the post-chronic exposure\nof Cd. This study encourages the field of post-exposure research which is crucial but has long\nbeen ignored.
Loading....