Chronic Exposure to Particulate Nickel Induces Neoplastic Transformation in Human Lung Epithelial Cells

Toxics

Amie L. Holmes²  Therry The²  Kelsey Thompson²  Michael Mason³  Sanjeev Kandpal³  Tongzhang Zheng¹ 

[1] Department of Environmental Health Sciences, Yale School of Public Health, New Haven, CT 06520, USA; E-Mail:;Wise Laboratory of Environmental and Genetic Toxicology, University of Southern Maine, Portland, ME 04104, USA; E-Mails:;Department of Chemical and Biological Engineering, University of Maine, Orono, ME 04469, USA; E-Mails:

关键词: particulate nickel;    nickel subsulfide;    chromosome damage;    transformation;   

DOI  :  10.3390/toxics1010046

来源: mdpi

【 摘 要 】

Nickel is a well-known human lung carcinogen with the particulate form being the most potent; however, the carcinogenic mechanism remains largely unknown. Few studies have investigated the genotoxicity and carcinogenicity of nickel in its target cell, human bronchial epithelial cells. Thus, the goal of this study was to investigate the effects of particulate nickel in human lung epithelial cells. We found that nickel subsulfide induced concentration- and time-dependent increases in both cytotoxicity and genotoxicity in human lung epithelial cells (BEP2D). Chronic exposure to nickel subsulfide readily induced cellular transformation, inducing 2.55, 2.9 and 2.35 foci per dish after exposure to 1, 2.5 and 5 μg/cm² nickel subsulfide, respectively. Sixty-one, 100 and 70 percent of the foci isolated from 1, 2.5, and 5 μg/cm² nickel subsulfide treatments formed colonies in soft agar and the degree of soft agar colony growth increased in a concentration-dependent manner. Thus, chronic exposure to particulate nickel induces genotoxicity and cellular transformation in human lung epithelial cells.

【 授权许可】

CC BY   
© 2013 by the authors; licensee MDPI, Basel, Switzerland.