Journal
FOOD AND CHEMICAL TOXICOLOGY
Volume 103, Issue -, Pages 157-167Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.fct.2017.03.014
Keywords
Di(2-ethylhexyl)phthalate; Colorectal cancer; beta-Catenin; Cyclooygenase-2; Vascular endothelial growth factor; Cyclin D1
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Funding
- Ministry of Science and Technology [MOST 104-2221-E-327-005-MY3]
- National Health Research Institutes of Taiwan [NHRI-105A1-PDCO-3316161]
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Di(2-ethylhexyl)phthalate (DEHP) may cause carcinogenicity in the liver; however, few have detailed on the potential effects of DEHP exposure on colorectal cancer. Male Sprague-Dawley rats received i.p. injections of 1,2-dimethylhydrazine (DMH) once-a-week for the first 4 weeks, and rats in each group were treated with DEHP through oral gavage daily for either 7, 10 or 15 weeks; after which, all rats were euthanized and their colons were assessed (a) morphologically for aberrant crypt foci (ACF) or tumors, (b) cytologically for mitotic index (MI), and (c) immunohistochemically for the expression of beta-catenin, cyclooygenase (COX)-2, vascular endothelial growth factor (VEGF), proliferating cell nuclear antigen (PCNA), cyclin D1, and c-myc. Our results indicated that the mean total ACF, tumor incidence, and MI were significantly higher in the DEHP-treated DMH compared to control and the DEHP-alone groups. The level of beta-catenin and cyclin D1 was increased in DEHP-exposed rats. Expression of beta-catenin, COX -2, VEGF, and cyclin D1 was significantly higher in the combined DMH and DEHP-treated rats by comparison to that of the DMH group. In conclusion, this study indicates that exposure to DEHP may exacerbate DMH-induced colon tumorigenesis and provides impetus to evaluate the effect of DEHP in conjunction with other carcinogens. (C) 2017 Elsevier Ltd. All rights reserved.
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