Mense Sarah M, Remotti Fabrizio, Bhan Ashima, Singh Bhupendra, El-Tamer Mahmoud, Hei Tom K, Bhat Hari K
Department of Environmental Health Science Mailman School of Public Health Columbia University, New York, NY 10032, USA.
Toxicol Appl Pharmacol. 2008 Oct 1;232(1):78-85. doi: 10.1016/j.taap.2008.06.007. Epub 2008 Jul 1.
Epidemiological evidence indicates that prolonged lifetime exposure to estrogen is associated with elevated breast cancer risk in women. Oxidative stress and estrogen receptor-associated proliferative changes are suggested to play important roles in estrogen-induced breast carcinogenesis. In the present study, we investigated changes in breast morphology and oxidative stress following estrogen exposure. Female ACI rats were treated with 17beta-estradiol (E(2), 3 mg, s.c.) for either 7, 15, 120 or 240 days. Animals were euthanized, tissues were excised, and portions of the tissues were either fixed in 10% buffered formalin or snap-frozen in liquid nitrogen. Paraffin-embedded tissues were examined for histopathologic changes. Proliferative changes appeared in the breast after 7 days of E(2) exposure. Atypical ductal proliferation and significant reduction in stromal fat were observed following 120 days of E(2) exposure. Both in situ and invasive carcinomas were observed in the majority of the mammary glands from rats treated with E(2) for 240 days. Palpable breast tumors were observed in 82% of E(2)-treated rats after 228 days, with the first palpable tumor appearing after 128 days. No morphological changes were observed in the livers, kidneys, lungs or brains of rats treated with E(2) for 240 days compared to controls. Furthermore, 8-isoprostane (8-isoPGF(2alpha)) levels as well as the activities of antioxidant enzymes, such as glutathione peroxidase, superoxide dismutase and catalase, were quantified in the breast tissues of rats treated with E(2) for 7, 15, 120 and 240 days and compared to activity levels in age-matched controls. 8-isoPGF(2alpha) levels displayed time-dependent increases upon E(2) treatment and were significantly higher than control levels at the 15, 120 and 240 day time-points. 8-isoPGF(2alpha) observed in E(2)-induced mammary tumors were significantly higher than levels found in control mammary tissue from age-matched animals. Similarly, alterations in glutathione peroxidase and superoxide dismutase activities were detected in both mammary and tumor tissue from E(2)-treated rats. Taken together, our data reveal that proliferative changes in the breast tissue of ACI rats are associated with increases in 8-isoPGF(2alpha) formation as well as changes in the activities of antioxidant enzymes. These oxidative changes appear to be a function of E(2) exposure and occur prior to tumor development.
流行病学证据表明,女性一生中长期暴露于雌激素与乳腺癌风险升高有关。氧化应激和雌激素受体相关的增殖性变化被认为在雌激素诱导的乳腺癌发生过程中起重要作用。在本研究中,我们调查了雌激素暴露后乳腺形态和氧化应激的变化。将雌性ACI大鼠用17β-雌二醇(E₂,3mg,皮下注射)处理7、15、120或240天。对动物实施安乐死,切除组织,部分组织用10%缓冲甲醛固定或在液氮中速冻。对石蜡包埋组织进行组织病理学变化检查。E₂暴露7天后乳腺出现增殖性变化。E₂暴露120天后观察到非典型导管增生和间质脂肪显著减少。在接受E₂处理240天的大鼠的大多数乳腺中观察到原位癌和浸润癌。在228天后,82%接受E₂处理的大鼠可触及乳腺肿瘤,第一个可触及肿瘤在128天后出现。与对照组相比,接受E₂处理240天的大鼠的肝脏、肾脏、肺或脑未观察到形态学变化。此外,对接受E₂处理7、15、120和240天的大鼠乳腺组织中的8-异前列腺素(8-isoPGF₂α)水平以及抗氧化酶如谷胱甘肽过氧化物酶、超氧化物歧化酶和过氧化氢酶的活性进行了定量,并与年龄匹配的对照组的活性水平进行比较。E₂处理后8-isoPGF₂α水平呈时间依赖性升高,在15、120和240天时间点显著高于对照水平。在E₂诱导的乳腺肿瘤中观察到的8-isoPGF₂α显著高于年龄匹配动物的对照乳腺组织中的水平。同样,在接受E₂处理的大鼠的乳腺和肿瘤组织中均检测到谷胱甘肽过氧化物酶和超氧化物歧化酶活性的改变。综上所述,我们的数据表明,ACI大鼠乳腺组织中的增殖性变化与8-isoPGF₂α形成增加以及抗氧化酶活性变化有关。这些氧化变化似乎是E₂暴露的结果,且发生在肿瘤发展之前。