Potential lung carcinogenicity induced by chronic exposure to PM2.5 in the rat

Potential lung carcinogenicity induced by chronic exposure to PM2.5 in the rat Exposure to fine particulate matter (PM2.5) 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 PM2.5. Adult male rats (200–220 g) were treated with PM2.5 (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 PM2.5 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 PM2.5 exposure. Chronic exposure to PM2.5 has the potential to be carcinogenic in rat lung. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Environmental Science and Pollution Research Springer Journals

Potential lung carcinogenicity induced by chronic exposure to PM2.5 in the rat

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Publisher
Springer Berlin Heidelberg
Copyright
Copyright © 2017 by Springer-Verlag GmbH Germany
Subject
Environment; Environment, general; Environmental Chemistry; Ecotoxicology; Environmental Health; Atmospheric Protection/Air Quality Control/Air Pollution; Waste Water Technology / Water Pollution Control / Water Management / Aquatic Pollution
ISSN
0944-1344
eISSN
1614-7499
D.O.I.
10.1007/s11356-017-9430-6
Publisher site
See Article on Publisher Site

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