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Published on: November 13, 2013
Nicotine exposure impairs germ cell development in human fetal ovaries cultured in vitro
Shun-Feng Cheng1, Xun-Si Qin1, Ze-Li Han2
1College of Life Sciences, Institute of Reproductive Sciences, Qingdao Agricultural University, Qingdao 266109, China.
Abstract:
In the present paper, we found that human fetal ovaries (at ~16 weeks) express the transcripts for several subunits of the nicotinic acetylcholine receptor (nAChR). Exposure to the drug in vitro resulted in the marked increase of apoptosis in the ovaries in a time and dose-dependent manner. Evidence that adverse nicotine effects are potentially due to an increased level of reactive oxygen species (ROS) and consequent DNA damage, both in the ovarian somatic cells and germ cells, are reported. After 4 days of culture, exposure to 1 mM and 10 mM nicotine caused a 50% and 75% decrease, respectively, in the number of oogonia/oocytes present in the fetal ovaries. These results represent the first indication that nicotine may directly cause apoptosis in cells of the fetal human ovary and may lead to a reduction of the ovarian reserve oocytes and consequent precocious menopause in mothers smoking during pregnancy.
Insights
Nicotine exposure in vitro induces apoptosis in human fetal ovaries by increasing reactive oxygen species (ROS). This can reduce ovarian reserve and potentially lead to premature menopause in infants born to mothers who smoked during pregnancy.
Area of Science:
- Reproductive Biology
- Developmental Toxicology
- Neuroscience
Background:
- Nicotinic acetylcholine receptors (nAChRs) are present in human fetal ovaries.
- Nicotine exposure during pregnancy is a significant concern for reproductive health.
- The direct impact of nicotine on fetal ovarian development is not fully understood.
Purpose of the Study:
- To investigate the direct effects of nicotine on human fetal ovarian cells.
- To determine the mechanisms underlying nicotine-induced ovarian cell damage.
- To assess the potential long-term consequences of prenatal nicotine exposure on ovarian reserve.
Main Methods:
- Human fetal ovaries (16 weeks gestation) were cultured in vitro.
- Ovaries were exposed to varying concentrations of nicotine.
- Apoptosis, reactive oxygen species (ROS) levels, and DNA damage were assessed.
- The number of oogonia/oocytes was quantified after nicotine treatment.
Main Results:
- Nicotine exposure increased apoptosis in fetal ovarian cells in a time- and dose-dependent manner.
- Nicotine exposure led to increased ROS production and DNA damage in ovarian somatic and germ cells.
- A significant reduction in oogonia/oocytes was observed following nicotine treatment (50% at 1 mM, 75% at 10 mM).
Conclusions:
- Nicotine directly induces apoptosis in human fetal ovarian cells.
- Nicotine exposure may deplete the ovarian reserve, potentially leading to premature menopause.
- This study highlights the risks of maternal smoking during pregnancy for female reproductive health.
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