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The effects of high dose progesterone on neural tube development in early chick embryos
Erdincler Pamir1, Dalgic Ali, Cepni Ismail
1Department of Gynecology and Obstetrics, Istanbul University, Cerrahpasa Medical Faculty, Turkey.
Insights
High doses of progesterone may cause neural tube defects (NTDs) in developing embryos. This study found that 20 times the normal progesterone level led to NTDs in chick embryos, suggesting a potential teratogenic effect.
Area of Science:
- Developmental Biology
- Reproductive Endocrinology
- Teratology
Background:
- Folic acid deficiency is a known risk factor for neural tube defects (NTDs), but the precise mechanisms remain unclear.
- Progesterone is a crucial endogenous hormone with significantly elevated levels during pregnancy.
Purpose of the Study:
- To investigate the potential adverse effects of high-dose progesterone exposure on early embryonic neural tube development.
- To test the hypothesis that elevated progesterone levels may contribute to NTD formation.
Main Methods:
- 160 fertile white leghorn eggs (Gallus gallus) at developmental stage eight were divided into four groups.
- Embryos were exposed to physiological saline, normal progesterone doses, or high progesterone doses (2x and 20x physiologic levels).
- Neural tube development and the presence of NTDs were assessed via light microscopy after 48 hours of incubation.
Main Results:
- 84% of embryos reached stage 12 development and were included in the analysis.
- No NTDs were observed in control groups (saline or normal progesterone).
- A significant incidence of NTDs (81.8%) was observed in embryos exposed to 20 times the physiologic progesterone dose.
Conclusions:
- Progesterone at supranational levels (20x physiologic) may act as a teratogen, inducing neural tube defects.
- Further research is warranted to elucidate the specific molecular mechanisms underlying progesterone's teratogenic potential in embryonic development.
Background:
Although folic acid deficiency is known to be one of the factors in the development of spina bifida and other neural tube defects (NTD) the exact pathophysiology still remains unclear. Progesterone is an endogenous hormone which increases significantly during pregnancy.
Aims:
We aimed to study the possible negative effects of high dose progesterone on neural tube development in early chick embryos. In order to test our hypothesis, early chick embryos were exposed to physiological saline, normal and high doses of progesterone.
Settings And Design:
160 fertile, specific pathogen free white leghorn eggs (Gallus gallus), all at stage eight of development were divided into four equal groups.
Materials And Methods:
The first group was incubated without any operation. The second group was injected with physiological saline. The third and fourth groups were injected with two and twenty times more than physiologic doses of progesterone respectively. After 48 hours of incubation, all embryos were analyzed for the presence of NTDs under light microscopy.
Statistical Analysis Used:
None.
Results:
At 48 hours of incubation, 84% (135/160) of the embryos passed characteristics of Stage 12 development and were included to the study. None of the eggs in the first three groups showed NTDs, whereas 81.8% (27/33) of the eggs in the fourth group showed NTDs.
Conclusions:
Our study showed that progesterone at levels twenty times more than its physiologic level might cause NTDs. Further studies are needed to explain the mechanisms of this teratogenic effect.
