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围生期雄激素过多会改变后代子宫中甾体激素受体的表达、细胞凋亡和细胞增殖。

Excess androgen during perinatal life alters steroid receptor expression, apoptosis, and cell proliferation in the uteri of the offspring.

机构信息

Graduate Program in Cell and Structural Biology, Institute of Biology, State University of Campinas-UNICAMP, Campinas, SP, Brazil.

出版信息

Reprod Toxicol. 2013 Sep;40:1-7. doi: 10.1016/j.reprotox.2013.05.001. Epub 2013 May 10.

Abstract

Exposure to environmental chemicals may contribute to reproductive disorders, especially when it occurs in critical periods of development. The female reproductive system can be a target for androgens derived from environmental contaminants or pathological conditions. The purpose of this study was to assess the long-term effects of androgens on uterine tissue after maternal exposure limited to the time of gestation and lactation. Pregnant Wistar rats were treated with testosterone propionate (TP) at 0.05 mg/kg, 0.1 mg/kg, 0.2 mg/kg or corn oil (vehicle), s.c., from gestational day 12 until the end of lactation. The results show changes in the pattern of expression of receptors for estrogen, progesterone, and androgen at all doses tested, and decreases in both apoptosis and cell proliferation indices at 0.1 and 0.2 mg/kg. We conclude that early TP exposure, under these experimental conditions, causes changes in cellular and molecular parameters that are essential for normal uterine function in the adult.

摘要

暴露于环境化学物质可能导致生殖系统疾病,尤其是在发育的关键时期。女性生殖系统可能成为源自环境污染物或病理状况的雄激素的靶标。本研究的目的是评估雄激素在母体仅在妊娠期和哺乳期暴露后的子宫组织中的长期作用。从妊娠第 12 天到哺乳期结束,用丙酸睾酮(TP)以 0.05mg/kg、0.1mg/kg、0.2mg/kg 或玉米油(载体)经皮下处理怀孕的 Wistar 大鼠。结果表明,在所有测试剂量下,雌激素、孕激素和雄激素受体的表达模式都发生了变化,并且在 0.1 和 0.2mg/kg 时细胞凋亡和细胞增殖指数均降低。我们得出结论,在这些实验条件下,早期 TP 暴露会导致正常成年子宫功能所必需的细胞和分子参数发生变化。

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