Department of Respiratory, Tianjin Medical University General Hospital, 54 Anshan Road, Heping District, Tianjin, Tianjin, 300052, China.
Department of Respiratory, People's Hospital of Qitaihe City, 37 Shanhu Road, Qitaihe, Heilongjiang, 154600, China.
Environ Sci Pollut Res Int. 2017 Aug;24(23):18991-19000. doi: 10.1007/s11356-017-9430-6. Epub 2017 Jun 28.
Exposure to fine particulate matter (PM) may increase lung cancer risk, but the underlying mechanisms are poorly understood. This study explored the potential carcinogenicity in rat lung induced by chronic exposure to PM. Adult male rats (200-220 g) were treated with PM (10 mg/kg body weight) by tracheal perfusion once per week for 1 year; the rats were killed, and expression of tumor markers (carcinoembryonic antigen (CEA), neuron-specific enolase (NSE), squamous cell carcinoma antigen (SCCA)), cancer-related genes, and pathological changes were detected. Chronic treatment with PM significantly increased SCCA and NSE expression in rat lung tissue and serum. Damaged lung tissue structure was observed by hematoxylin and eosin staining. Although no evidence of tumors was detected, the Wnt/β-catenin signaling, epithelial-mesenchymal transition, vascular endothelial growth factor, and epidermal growth factor receptor pathways were all activated or overexpressed and likely involved in the potential carcinogenicity in the rat model. Additionally, abnormal expression of the proto-oncogenes c-Myc and K-Ras and tumor suppressor p53 can be seen in lung tissue induced by PM exposure. Chronic exposure to PM has the potential to be carcinogenic in rat lung.
暴露于细颗粒物（PM）可能会增加肺癌风险，但潜在机制尚不清楚。本研究探讨了慢性 PM 暴露对大鼠肺部的潜在致癌性。成年雄性大鼠（200-220g）通过气管灌注每周接受一次 PM（10mg/kg 体重）处理，持续 1 年；处死大鼠，检测肿瘤标志物（癌胚抗原（CEA）、神经元特异性烯醇化酶（NSE）、鳞状细胞癌抗原（SCCA））、癌症相关基因和组织病理学变化。慢性 PM 处理显著增加了大鼠肺组织和血清中 SCCA 和 NSE 的表达。苏木精和伊红染色观察到受损的肺组织结构。尽管未检测到肿瘤证据，但 Wnt/β-catenin 信号通路、上皮-间充质转化、血管内皮生长因子和表皮生长因子受体通路均被激活或过度表达，可能参与了大鼠模型中的潜在致癌性。此外，还可以看到 PM 暴露诱导的肺组织中原癌基因 c-Myc 和 K-Ras 以及肿瘤抑制基因 p53 的异常表达。慢性 PM 暴露有可能在大鼠肺部致癌。
