Dietary Selenium Supplement Prevents Colon Carcinogenesis Induced by Azoxymethane and Dextran Sodium Sulfate in ICR Mice.
10.5625/lar.2010.26.3.293
- Author:
Jun Hyeong KIM
1
;
Jin Joo HUE
;
Bong Su KANG
;
Hyunji PARK
;
Sang Yoon NAM
;
Young Won YUN
;
Jong Soo KIM
;
Jae Hwang JEONG
;
Beom Jun LEE
Author Information
1. Department of Veterinary Medicine, College of Veterinary Medicine and Research Institute of Veterinary Medicine, Chungbuk National University, Cheongju, Korea. beomjun@cbu.ac.kr
- Publication Type:Original Article
- Keywords:
Azoxymethane (AOM);
dextran sodium sulfate (DSS);
colon cancer;
selenium;
cell proliferation;
apoptosis
- MeSH:
Animals;
Apoptosis;
Azoxymethane;
Blood Cells;
Cell Proliferation;
Colon;
Colonic Neoplasms;
Dextrans;
Diet;
Drinking Water;
Hematology;
Humans;
Incidence;
Injections, Intraperitoneal;
Liver;
Male;
Mice;
Mice, Inbred ICR;
Organothiophosphorus Compounds;
Proliferating Cell Nuclear Antigen;
Selenium;
Sodium;
Spectrum Analysis;
Sulfates
- From:Laboratory Animal Research
2010;26(3):293-300
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
The role of selenium (Se) in modulating colon carcinogenesis induced by azoxymethane (AOM) followed by dextran sodium sulfate (DSS) was investigated in mice. Five-week old ICR mice were fed on diets containing different concentrations (0.02, 0.1 or 0.5 ppm) of Se for 24 weeks. Animals received three (0-2nd weeks) intraperitoneal injections of AOM (10 mg/kg body weight), followed by 2% DSS with drinking water for additional 1 week. There were 4 experimental groups including vehicle control group, positive control group given AOM/DSS with AIN-93G normal diet containing 0.1% Se (NSe), a low (0.02 ppm)-Se diet group (LSe) and a high (0.5 ppm)-Se diet group (HSe). Hematology was analyzed with a blood cell differential counter. Liver Se was analyzed by inductively coupled plasma-mass spectroscopy. Cell proliferation and apoptosis were determined by using proliferating cell nuclear antigen (PCNA) for proliferative activity and apoptotic index by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL), respectively. HSe group showed a low incidence of colonic tumor (64.7%), compared with the NSe positive control (75%) and LSe (77.8%) groups. In contrast, HSe group exhibited lower rate of PCNA-positive cells (39.3+/-6.9%) than positive control (64.3+/-0.3%) and LSe (57.3+/-2.9%) groups. In addition, apoptotic index of HSe group was higher than those of positive control and LSe groups. These results indicate that Se is a chemopreventive agent for colon carcinogenesis induced by AOM+DSS in male ICR mice.
