Effects of co-treatment of dextran sulfate sodium and MeIQx on genotoxicity and possible carcinogenicity in the colon of p53-deficient mice

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  • Okamura Toshiya
    Division of Pathology, National Institute of Health Sciences Pathogenetic Veterinary Science, United Graduate School of Veterinary Sciences, Gifu University
  • Ishii Yuji
    Division of Pathology, National Institute of Health Sciences
  • Suzuki Yuta
    Division of Pathology, National Institute of Health Sciences
  • Inoue Tomoki
    Division of Pathology, National Institute of Health Sciences
  • Tasaki Masako
    Division of Pathology, National Institute of Health Sciences
  • Kodama Yukio
    Division of Toxicology, National Institute of Health Sciences
  • Nohmi Takehiko
    Division of Genetics and Mutagenesis, National Institute of Health Sciences
  • Mitsumori Kunitoshi
    Laboratory of Veterinary Pathology, Tokyo University of Agriculture and Technology
  • Umemura Takashi
    Division of Pathology, National Institute of Health Sciences
  • Nishikawa Akiyoshi
    Division of Pathology, National Institute of Health Sciences

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To investigate the effects of dextran sulfate sodium (DSS) and/or 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (MeIQx) on in vivo genotoxicity in the colon, male C57BL/6 p53 (+/+), p53 (+/-) or p53 (-/-) gpt delta mice were twice given 1-week treatment with DSS, 2 weeks apart, and then sacrificed after 2 and 14 weeks. Although colon length was significantly shortened after DSS treatment in all genotypes at each time point, no significant difference in gpt mutant frequency (MF) and tumorigenicity was found between DSS and control groups regardless of genotype. Then, male B6C3F1 p53 (+/+) or p53 (+/-) gpt delta mice were given DSS as described above and/or fed 300 ppm MeIQx for 7 weeks. Colon length was significantly shortened with DSS in either genotype at weeks 7 and 26, but no effects of co-treatment with MeIQx or p53 deficiency were evident. MeIQx showed a tendency to increase gpt MF in the colon of mice with either genotype, but co-treatment with DSS did not affect these increments. Appreciable incidences of colonic aberrant crypt foci (ACFs) were reported in DSS as well as co-treatment groups of each genotype. Colonic adenomas were observed in co-treatment groups of both genotypes as well as the DSS-only group of p53 (+/+). No effects of the combination of DSS and MeIQx on colon pre- and neoplastic lesions were reported. Our results indicate that MeIQx may take more than 7 weeks to induce genotoxicity in the colon and that the co-treatment of mice did not enhance colon tumorigenicity even in p53-deficient mice.

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