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Published on: July 7, 2014
Oxidative stress induced by methomyl exposure reduces the quality of early embryo development in mice
Daohong He1,2, Guobo Han1,2, Xiaomeng Zhang1,2
1College of Agriculture, Yanbian University, Yanji, 133000China.
Abstract:
Methomyl is a widely used carbamate insecticide and environmental oestrogen that has adverse effects on the reproductive system. However, there have been no reports on the effect of methomyl on early embryos in mammals. In this study, we explored the effect of methomyl exposure on the quality of early embryonic development in mice and the possible mechanisms. During in vitro culture, different concentrations of methomyl (10, 20, 30 and 35 μM) were added to mouse zygote medium. The results showed that methomyl had an adverse effect on early embryonic development. Compared with the control group, the addition of 30 μM methomyl significantly reduced the rate of early embryo blastocyst formation. Methomyl exposure can increase oxidative stress and impair mitochondrial function, which may be the cause of blastocyst formation. In addition, we found that methomyl exposure promoted apoptosis and autophagy in mouse blastocysts. The toxic effect of methomyl on early embryos may be the result of oxidative stress induction. Taken together, our results indicate that methomyl can cause embryonic development defects in mice, thereby reducing the quality of early embryo development.
Insights
Methomyl, a carbamate insecticide, harms early mouse embryo development by increasing oxidative stress and impairing mitochondrial function. This toxic effect reduces blastocyst formation and overall embryo quality.
Area of Science:
- Reproductive toxicology
- Developmental biology
- Environmental health
Background:
- Methomyl is a common carbamate insecticide with known reproductive toxicity.
- Environmental oestrogens like methomyl can disrupt endocrine systems.
- Limited data exists on methomyl's impact on mammalian early embryonic development.
Purpose of the Study:
- To investigate the effects of methomyl exposure on mouse early embryonic development.
- To elucidate the underlying mechanisms of methomyl's toxicity on embryos.
- To assess methomyl's impact on blastocyst formation and quality.
Main Methods:
- In vitro culture of mouse zygotes with varying methomyl concentrations (10–35 μM).
- Assessment of early embryonic development, including blastocyst formation rates.
- Analysis of oxidative stress, mitochondrial function, apoptosis, and autophagy in blastocysts.
Main Results:
- Methomyl exposure adversely affected early embryonic development in a dose-dependent manner.
- A significant reduction in blastocyst formation rate was observed at 30 μM methomyl.
- Methomyl increased oxidative stress, impaired mitochondrial function, and promoted apoptosis and autophagy in mouse blastocysts.
Conclusions:
- Methomyl exposure causes embryonic developmental defects in mice.
- Oxidative stress induction is a key mechanism underlying methomyl's toxicity to early embryos.
- Methomyl reduces the quality of early embryonic development, impacting reproductive potential.
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