As a possible carcinogen, carbon black has threatened public health. However, the evidences are insufficient and the mechanism of carcinogenesis is still not specified. Thirty rats were randomly divided into 3 groups, namely 0, 5 and 30 mg/m3 Carbon Black nanoparticles (CBNPs) groups, respectively. Rats were treated with CBNPs by nose-only inhalation for 28 days, 6 h/day. The human bronchial epithelial (16HBE) cells were treated with 0, 50, 100 and 200 μg/mL CBNPs for 24 h. Polo-like kinase 1 (PLK1) overexpression cell line was established by pcDNA3.1-PLK1 stable transfection. Our results showed that CBNPs exposure could induce DNA damage and genetic changes as well as apoptosis in vivo and in vitro. The DNA repair ability increased after CBNPs exposure. Cell cycle process was retarded at the G2/M phases in 16HBE cells after CBNPs treatment. The PLK1, ChK2 GADD45α and XRCC1 expression levels changed in rat lung and 16HBE cells after CBNPs treatment. Compared with NC 16HBE cells, DNA damage and repair, numbers of apoptotic cells and micronucleus (MN) rates, as well as the ChK2, GADD45α, XRCC1 expression levels decreased, whereas cytokinesis block proliferation index (CBPI) and replicative index (RI) increase in PLK overexpression (PLK+/+) cells after CBNPs treatment. This study highlighted that PLK1 related with the genetic toxicity of CBNPs in vitro and in vivo. Our results provided evidences supporting reclassification of carbon black as a human possible carcinogen.
Keywords: Carbon black nanoparticles (CBNPs); DNA damage; Genomic instability; PLK1; Pulmonary toxicity.
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