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Updated: Aug 12, 2026
Ovariectomy and 17β-estradiol Replacement in Rats and Mice: A Visual Demonstration
Published on: June 7, 2012
Oestradiol, cyclodextrin-encapsulated 17beta-oestradiol and the oestradiol solubilizer
Levent Karagenc1, Michelle Lane, David K Gardner
1Bahceci Women Health Care Centre and German Hospital in Istanbul. leventkaragenc@yahoo.com
Abstract:
The aim of this study was to examine the effects of 2-hydroxypropyl-beta-cyclodextrin (HbetaC) used as a solubilizer for oestradiol, 17beta-oestradiol (ethanol soluble) and HbetaC-encapsulated-17beta-oestradiol on mouse embryo development in vitro. HbetaC had no effect on day 3 development. In contrast, blastocyst development and blastocyst cell number were significantly reduced in the presence of 10(-4) mol/l solubilizer equivalent, but not at lower concentrations. The proportion of compacted embryos was significantly reduced with 10(-4) mol/l 17beta-oestradiol. No blastocysts were formed at 10(-4) mol/l concentration of 17beta-oestradiol, although the rate of blastocyst formation did not differ at lower concentrations. Blastocyst cell number was significantly decreased compared with controls at 10(-5) mol/l 17beta-oestradiol. The dose-response using HbetaC-encapsulated-17beta-oestradiol revealed that at 17beta-oestradiol concentrations of 10(-4) and 10(-5) mol/l, blastocyst development was significantly reduced. Blastocyst cell number was significantly reduced compared with controls for all concentrations of HbetaC-encapsulated-17beta-oestradiol. Exposure of embryos to 17beta-oestradiol (10(-4) mol/l) reduced blastocyst development on days 4 and 5 significantly in cultures initiated at the zygote, 2-cell and 8-cell, but not the morulae, stages of development. Trophectoderm, ICM and blastocyst cell numbers as well as percentage ICM development were reduced significantly, regardless of the stage of development. Therefore, 17beta-oestradiol does compromise embryo development.
Insights
High concentrations of 17beta-oestradiol, whether free or encapsulated with 2-hydroxypropyl-beta-cyclodextrin (HbetaC), significantly impair mouse embryo development, reducing blastocyst formation and cell numbers.
Area of Science:
- Reproductive biology
- Developmental toxicology
- Biochemistry
Background:
- 17beta-oestradiol is a key hormone in reproduction.
- Cyclodextrins like 2-hydroxypropyl-beta-cyclodextrin (HbetaC) are used to improve drug solubility.
- The impact of solubilized or encapsulated 17beta-oestradiol on early embryo development requires investigation.
Purpose of the Study:
- To evaluate the in vitro effects of HbetaC-solubilized and HbetaC-encapsulated 17beta-oestradiol on mouse embryo development.
- To determine dose-dependent toxicity of 17beta-oestradiol on embryos at various developmental stages.
Main Methods:
- Mouse embryos at different stages (zygote to morula) were cultured in vitro.
- Embryos were exposed to varying concentrations of 17beta-oestradiol, HbetaC, and HbetaC-encapsulated 17beta-oestradiol.
- Blastocyst development, cell counts (trophectoderm, ICM), and compaction rates were assessed.
Main Results:
- HbetaC alone did not affect early embryo development.
- High concentrations (10(-4) mol/l) of 17beta-oestradiol significantly reduced blastocyst formation and cell numbers.
- Both free and HbetaC-encapsulated 17beta-oestradiol compromised blastocyst development and cell counts, with effects observed at 10(-5) mol/l for encapsulated forms.
Conclusions:
- 17beta-oestradiol, particularly at higher concentrations, exerts a detrimental effect on mouse embryo development in vitro.
- HbetaC encapsulation does not mitigate the negative impact of 17beta-oestradiol on embryo development.
- These findings highlight the potential reproductive toxicity of 17beta-oestradiol.
