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Updated: May 3, 2026
Mouse Oocyte Microinjection, Maturation and Ploidy Assessment
Published on: July 23, 2011
Methylglyoxal has injurious effects on maturation of mouse oocytes, fertilization, and fetal development, via
Ying-Jing Chang1, Wen-Hsiung Chan
1Department of Bioscience Technology, Center for Nanotechnology, Chung Yuan Christian University, Chung Li, Taiwan.
Abstract:
Methylglyoxal (MG) is a metabolite of glucose. The serum MG level is increased in diabetic patients, and MG is implicated in diabetic complications related to embryonic development injury. We previously reported cytotoxic effects of MG on mouse embryonic stem cells and blastocysts, and a further association with defects in subsequent development. Here, we further investigate the effects of MG on oocyte maturation and subsequent pre- and post-implantation development, both in vitro and in vivo. Notably, MG induced a significant reduction in the rate of oocyte maturation, fertilization, and in vitro embryonic development. Treatment of oocytes with MG during in vitro maturation (IVM) led to increased resorption of post-implantation embryos and decreased fetal weight. Experiments with an in vivo mouse model disclosed that consumption of drinking water containing 10-20 microM MG led to decreased oocyte maturation and in vitro fertilization, as well as early embryonic developmental injury. Finally, pretreatment with a caspase-3-specific inhibitor effectively prevented MG-triggered injury effects, suggesting that embryo impairment by MG occurs via a caspase-dependent apoptotic process.
Insights
High methylglyoxal (MG) levels impair female fertility. This study shows MG negatively impacts oocyte maturation, fertilization, and embryonic development, potentially through apoptosis.
Area of Science:
- Reproductive biology
- Developmental toxicology
- Metabolic disorders
Background:
- Methylglyoxal (MG), a glucose metabolite, is elevated in diabetes.
- Elevated MG is linked to diabetic complications, including embryonic developmental injury.
- Previous studies demonstrated MG's cytotoxicity to early embryonic cells.
Purpose of the Study:
- To investigate the impact of MG on oocyte maturation and subsequent embryonic development.
- To assess MG's effects both in vitro and in vivo.
- To elucidate the mechanism underlying MG-induced embryonic impairment.
Main Methods:
- In vitro maturation (IVM) of oocytes with MG exposure.
- Assessment of fertilization and in vitro embryonic development rates.
- In vivo mouse model with MG-containing drinking water.
- Evaluation of post-implantation development and fetal parameters.
- Caspase-3 inhibitor treatment to assess apoptosis.
Main Results:
- MG significantly reduced oocyte maturation, fertilization, and in vitro embryonic development rates.
- In vitro maturation with MG exposure resulted in increased embryo resorption and decreased fetal weight.
- In vivo MG exposure impaired oocyte maturation, fertilization, and early embryonic development.
- MG-induced embryonic injury was prevented by a caspase-3 inhibitor.
Conclusions:
- Methylglyoxal negatively affects oocyte quality and early embryonic development.
- MG-induced developmental toxicity in embryos appears to be mediated by caspase-dependent apoptosis.
- These findings highlight the detrimental role of hyperglycemia-associated metabolites in reproductive health.
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