Laboratory of Hygienic Chemistry and Molecular Toxicology, Gifu Pharmaceutical University, Gifu, Japan.
J Toxicol Sci. 2010 Apr;35(2):225-30. doi: 10.2131/jts.35.225.
The purpose of this study was to examine whether intracellular metallothionein (MT) protects against benzo[a]pyrene (B[a]P)-induced forestomach and lung carcinogenesis. Ten-week-old male MT-I/II null mice and wild-type mice were orally administered B[a]P at a dose of 100 or 250 mg/kg twice a week for 4 weeks. B[a]P-induced mortality was higher in the MT-I/II null mice than in the wild-type mice. The incidence of tumors in the forestomach and lung was 78.6% and 7.1% in the wild-type mice treated with 100 mg/kg B[a]P, respectively. In the MT-I/II null mice treated with B[a]P, tumor incidence in the forestomach and lung was 100% and 33.3%, respectively. The tumor area in the forestomach and lung in the MT-I/II null mice treated with B[a]P was greater than that of wild-type mice. These results suggest that MT acts as a biological protective factor against carcinogenesis induced by B[a]P.
本研究旨在探讨细胞内金属硫蛋白 (MT) 是否能抵抗苯并[a]芘 (B[a]P) 诱导的前胃和肺癌发生。10 周龄雄性 MT-I/II 基因敲除小鼠和野生型小鼠每周两次口服给予 B[a]P，剂量为 100 或 250mg/kg，连续 4 周。MT-I/II 基因敲除小鼠的 B[a]P 诱导死亡率高于野生型小鼠。在接受 100mg/kg B[a]P 处理的野生型小鼠中，前胃和肺的肿瘤发生率分别为 78.6%和 7.1%。在接受 B[a]P 处理的 MT-I/II 基因敲除小鼠中，前胃和肺的肿瘤发生率分别为 100%和 33.3%。与野生型小鼠相比，接受 B[a]P 处理的 MT-I/II 基因敲除小鼠的前胃和肺肿瘤面积更大。这些结果表明 MT 作为一种生物保护因子，能抵抗 B[a]P 诱导的致癌作用。
