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首页> 外文期刊>The Journal of toxicological sciences >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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Effects of co-treatment of dextran sulfate sodium and MeIQx on genotoxicity and possible carcinogenicity in the colon of p53 -deficient mice

机译：硫酸葡聚糖钠和MeIQx联合处理对p53缺陷小鼠结肠遗传毒性和可能致癌性的影响

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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.
机译：研究硫酸葡聚糖硫酸钠（DSS）和/或2-氨基-3,8-二甲基咪唑并[4,5-f]喹喔啉（MeIQx）对结肠中雄性C57BL / 6 p53的体内遗传毒性的影响（+ / +），p53（+/-）或p53（-/-）gpt delta小鼠接受DSS 1周治疗两次，间隔2周，然后在2周和14周后处死。尽管在每个时间点所有基因型的DSS治疗后结肠长度均显着缩短，但无论基因型如何，DSS与对照组之间的gpt突变频率（MF）和致癌性均无显着差异。然后，对雄性B6C3F 1 p53（+ / +）或p53（+/-）gpt delta小鼠如上所述给予DSS和/或以300 ppm MeIQx喂养7周。在第7周和第26周，DSS在任一基因型下的结肠长度均显着缩短，但与MeIQx或p53缺乏症共同治疗的效果未见明显。 MeIQx在任一基因型小鼠的结肠中均显示出增加gpt MF的趋势，但与DSS共同治疗并不影响这些增加。在DSS以及每种基因型的联合治疗组中报告了结肠畸形隐窝灶（ACF）的明显发生率。在两种基因型的共同治疗组以及p53（+ / +）的仅DSS组中均观察到结肠腺瘤。没有报道DSS和MeIQx组合对结肠癌前病变和肿瘤病变的影响。我们的结果表明，MeIQx可能需要超过7周的时间才能在结肠中诱发基因毒性，并且小鼠的共同治疗即使在p53缺陷型小鼠中也不会增强结肠的致瘤性。

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