Dietary zinc inhibits the formation of colonic preneoplastic lesion induced by azoxymethane and dextran sodium sulfate in mice.
- Author:
Hyunji PARK
1
;
Dang Young KIM
;
Bong Su KANG
;
Ja Seon YOON
;
Jae Hwang JEONG
;
Sang Yoon NAM
;
Young Won YUN
;
Jong Soo KIM
;
Beom Jun LEE
Author Information
1. College of Veterinary Medicine and Research Institute of Veterinary Medicine, Chungbuk National University, Cheongju 361-763, Korea. beomjun@cbu.ac.kr
- Publication Type:Original Article
- Keywords:
aberrant crypt foci;
colon carcinogenesis;
mouse;
zinc
- MeSH:
Aberrant Crypt Foci;
Animals;
Azoxymethane;
beta Catenin;
Colon;
Colorectal Neoplasms;
Cytosol;
Developed Countries;
Dextrans;
Lipid Peroxidation;
Mice;
Mice, Inbred ICR;
Mucous Membrane;
Sodium;
Sulfates;
Superoxide Dismutase;
Thiobarbiturates;
Zinc
- From:Korean Journal of Veterinary Research
2012;52(2):115-124
- CountryRepublic of Korea
- Language:English
-
Abstract:
Colorectal cancer (CRC) is one of the leading causes of cancer death in western countries or in the developed countries. Zinc intake has been associated with decreased risk of CRC. We investigated the effect of zinc on the formation of colonic aberrant crypt foci (ACF) induced by azoxymethane followed by dextran sodium sulfate in mice. Five-week old ICR mice were fed with the different zinc levels (0.01, 0.1, 1 ppm) for 12 weeks. The numbers of ACF were measured in the colonic mucosa. The ACF number of HZn group was significantly low compared with LZn group or MZn group. Cytosolic superoxide dismutase activity was the highest in HZn group, while thiobarbituric acid reactive substance level for lipid peroxidation was the highest in LZn group. There was no difference in number of PCNA-positive proliferative cells among the groups. TUNEL-positive apoptotic cells were increased in HZn group compared with LZn group. The HZn group exhibited a decrease of beta-catenin immunostaining areas compared with the LZn or MZn group. These findings indicate that dietary zinc might exert a protecting effect against colon carcinogenesis by inhibiting the development of ACF in the mice.
