Colorectal Cancer
Copyright ©The Author(s) 2004. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Jan 15, 2004; 10(2): 218-222
Published online Jan 15, 2004. doi: 10.3748/wjg.v10.i2.218
Ethylene diamine tetraacetic acid induced colonic crypt cell hyperproliferation in rats
Qing-Yong Ma, Kate E Williamson, Brian J Rowlands
Qing-Yong Ma, Department of Surgery, First Hospital of Xi’an Jiaotong University, Xi’an 710061, Shaanxi Province, China
Kate E Williamson, Department of Pathology, Institute of Clinical Science, The Queen’s University of Belfast, Belfast, UK
Brian J Rowlands, Department of Surgery, School of medical and Surgical Sciences, University of Nottingham, Nottingham, NG7 2UH, UK
Author contributions: All authors contributed equally to the work.
Supported by DHSS of Northern Ireland
Correspondence to: Professor Qing-Yong Ma, Department of Surgery, First Hospital of Xi’an Jiaotong University, Xi’an 710061, Shaanxi Province, China. qyma0@163.com
Telephone: +86-29-85324009
Received: June 5, 2003
Revised: August 9, 2003
Accepted: August 16, 2003
Published online: January 15, 2004
Abstract

AIM: To investigate the effect of ethylene diamine tetraacetic acid (EDTA) on proliferation of rat colonic cells.

METHODS: EDTA was administered into Wistar rats, carcinogenesis induced by 1,2-dimethylhydrazine (DMH) in rats was studied with immunohistochemistry.

RESULTS: Marked regional differences in cell proliferation were found in all groups. In EDTA-treated animals, total labelling indexes in both proximal (10.00 ± 0.44 vs 7.20 ± 0.45) and distal (11.05 ± 0.45 vs 8.65 ± 0.34) colon and proliferative zone size (21.67 ± 1.13 vs 16.75 ± 1.45, 27.73 ± 1.46 vs 21.74 ± 1.07) were significantly higher than that in normal controls (P < 0.05) and lower than that in DMH group (10.00 ± 0.44 vs 11.54 ± 0.45, 11.05 ± 0.45 vs 13.13 ± 0.46, 21.67 ± 1.13 vs 35.52 ± 1.58, 27.73 ± 1.46 vs 39.61 ± 1.32, P < 0.05). Cumulative frequency distributions showed a shift of the EDTA distal curve to the right (P < 0.05) while the EDTA proximal curve did not change compared to normal controls. Despite the changes of proliferative parameters, tumours did not develop in EDTA treated animals.

CONCLUSION: Hyperproliferation appears to be more easily induced by EDTA in distal colon than in proximal colon. Hyperproliferation may need to exceed a threshold to develop colonic tumours. EDTA may work as a co-factor in colonic tumorigenesis.

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