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Effects of testosterone on rat placental development
Satoshi Furukawa1, Naho Tsuji1, Seigo Hayashi1
1Biological Research Laboratories, Nissan Chemical Corporation, 1470 Shiraoka, Shiraoka-shi, Saitama 349-0294, Japan.
Journal of Toxicologic Pathology
|February 28, 2022
Summary
High testosterone levels in pregnant rats with polycystic ovarian syndrome (PCOS) caused smaller placentas and fetal growth issues. This suggests testosterone inhibits placental development, impacting fetal growth.
Area of Science:
- Reproductive biology
- Developmental toxicology
- Endocrinology
Background:
- Polycystic ovarian syndrome (PCOS) is linked to hormonal imbalances, including elevated androgens.
- Maternal androgen excess during pregnancy may affect fetal development and placental function.
- Understanding these effects is crucial for managing pregnancy complications in women with PCOS.
Purpose of the Study:
- To investigate the impact of testosterone administration on placental morphology and development in a rat model of PCOS.
- To determine the timing and nature of placental changes induced by testosterone exposure.
Main Methods:
- Pregnant rats were administered testosterone propionate (TP) from gestation day (GD) 14 to GD 18.
- Maternal and fetal parameters, including weight and intrauterine growth retardation (IUGR) rates, were assessed.
- Placental histology and morphology were examined at GD 15, 17, and 21.
Main Results:
- TP administration led to maternal weight reduction but no mortality.
- A significant decrease in fetal and placental weight and increased IUGR rates were observed on GD 21.
- Histological analysis on GD 21 revealed thickened trophoblast septa and narrowed maternal sinusoids in the labyrinth zone, consistent with placental underdevelopment.
- These placental changes on GD 21 mirrored those observed on GD 17, suggesting developmental inhibition from GD 17 onwards.
Conclusions:
- Maternal testosterone excess in a PCOS rat model inhibits placental development, primarily affecting the fetal component from GD 17 onwards.
- This inhibition results in smaller placentas and contributes to intrauterine growth retardation.
- The findings highlight the potential adverse effects of androgen excess on pregnancy outcomes.
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