Department of Health and Environment, Institute of Health and Environmental Medicine, Key Laboratory of Risk Assessment and Control for Environment & Food Safety, Tianjin, PR China.
Cancer Lett. 2011 Sep 1;308(1):14-22. doi: 10.1016/j.canlet.2011.04.007. Epub 2011 May 23.
Estrogen may contribute to the development of smoking-induced lung cancer in women. To test this hypothesis, an mouse model was used to investigate the effects of 17 beta-estradiol (E2) on benzo[a]pyrene (B[a]P)-induced lung carcinogenesis. We found that B[a]P could cause oxidative stress damage, upregulate mitochondrial cytochrome-c and caspase-3 expression, induce lung carcinogenesis in female mice, E2 promoted these effects of B[a]P while tamoxifen (TAM) inhibited this effects of E2. We conclude that E2 can promote the tumorigenic effects of B[a]P in female mice, and oxidative stress damage and activation of cytochrome-c-mediated caspase-3 pathway may be involved in this process.
雌激素可能有助于女性吸烟引起的肺癌的发展。为了验证这一假说，使用一种小鼠模型来研究 17β-雌二醇（E2）对苯并[a]芘（B[a]P）诱导的肺癌发生的影响。我们发现，B[a]P 可以引起氧化应激损伤，上调线粒体细胞色素-c 和半胱氨酸蛋白酶-3 的表达，诱导雌性小鼠肺癌发生，E2 促进了这些 B[a]P 的作用，而他莫昔芬（TAM）抑制了 E2 的作用。我们的结论是，E2 可以促进雌性小鼠中 B[a]P 的致癌作用，而氧化应激损伤和细胞色素-c 介导的半胱氨酸蛋白酶-3 通路的激活可能参与了这一过程。
