Epigallocatechin gallate induces embryonic toxicity in mouse blastocysts through apoptosis
Yu-Ching Fan1, Wen-Hsiung Chan
1Department of Bioscience Technology and Center for Nanotechnology and.
Abstract:
Catechins, a family of polyphenols found in tea, evoke various responses, including cell death. However, the side effects of these compounds, particularly those on embryonic development, have not been characterized in detail. A previous study by our group showed that (-)-epigallocatechin-3-gallate (EGCG), a catechin highly abundant in green tea, induces different cell-death modes in MCF-7 cells, depending on the treatment dosage. In the current study, we examined the effects of EGCG on mouse embryos at the blastocyst stage, subsequent embryonic attachment and outgrowth in vitro and in vivo implantation by embryo transfer. Blastocysts treated with 25-50 μM of EGCG exhibited a significant increase in apoptosis and a corresponding decrease in total cell number. Notably, the implantation success rate of blastocysts pretreated with EGCG was lower than that of their control counterparts. Moreover, in vitro treatment with 25-50 μM of EGCG led to increased resorption of postimplantation embryos and decreased fetal weight. EGCG appeared to induce injury in mouse blastocysts through intrinsic apoptotic signaling processes to impair sequent embryonic development. These results collectively highlight the potential of EGCG to induce embryonic cytotoxicity.
Insights
(-)-Epigallocatechin-3-gallate (EGCG) from green tea can harm early mouse embryo development. This catechin increases apoptosis and reduces implantation success and fetal weight, indicating potential embryonic cytotoxicity.
Area of Science:
- Reproductive biology
- Developmental toxicology
- Cell biology
Background:
- Tea catechins, like (-)-epigallocatechin-3-gallate (EGCG), are known to induce cell death.
- The impact of EGCG on embryonic development and its potential side effects remain largely uncharacterized.
- Previous research indicated EGCG dosage-dependent cell death in cancer cells.
Purpose of the Study:
- To investigate the effects of EGCG on mouse embryos at the blastocyst stage.
- To assess EGCG's impact on embryonic attachment, outgrowth, and in vivo implantation.
- To determine the underlying mechanisms of EGCG-induced embryonic cytotoxicity.
Main Methods:
- Mouse blastocysts were treated with varying concentrations of EGCG (25-50 μM).
- Assessed apoptosis and cell number in treated blastocysts.
- Evaluated in vitro embryonic attachment and outgrowth, and in vivo implantation success via embryo transfer.
Main Results:
- EGCG treatment (25-50 μM) significantly increased blastocyst apoptosis and decreased total cell number.
- Pre-treatment with EGCG reduced the in vivo implantation success rate of blastocysts.
- In vitro exposure to EGCG resulted in increased postimplantation embryo resorption and reduced fetal weight.
Conclusions:
- EGCG induces cytotoxicity in mouse blastocysts, primarily through intrinsic apoptotic signaling pathways.
- EGCG impairs subsequent embryonic development, affecting implantation and fetal growth.
- These findings highlight the potential teratogenic risks associated with EGCG exposure during early embryonic development.
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