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Fenoxaprop-ethyl affects mouse oocyte quality and the underlying mechanisms
Ya-Ting He1, Lei-Lei Yang1, Yong Zhao1
1College of Animal Science and Technology, College of Life Sciences, Institute of Reproductive Sciences, Qingdao Agricultural University, Qingdao, China.
Pest Management Science
|August 29, 2018
Summary
Fenoxaprop-ethyl herbicide exposure harms female mice oocytes, impairing quality and fertilization. This occurs through disrupted cytoskeletal integrity and mitochondrial dysfunction, leading to oxidative stress and cell death.
Area of Science:
- Reproductive Toxicology
- Environmental Health
- Molecular Biology
Background:
- Fenoxaprop-ethyl (FE) is a widely used herbicide with known environmental and health risks.
- Limited information exists on the specific impact of FE on female reproductive health and underlying mechanisms.
Purpose of the Study:
- To investigate the toxic effects of fenoxaprop-ethyl (FE) on oocyte quality in female mice.
- To elucidate the mechanisms by which FE exposure affects oocyte maturation and fertilization potential.
Main Methods:
- Mice were fed a diet containing fenoxaprop-ethyl (FE).
- Oocyte quality was assessed by examining polar body extrusion and in vivo fertilization rates.
- Cytoskeletal integrity (actin expression, meiotic spindle morphology), mitochondrial function (ROS levels), apoptosis, autophagy, and epigenetic modifications (histone methylation) were analyzed.
Main Results:
- FE exposure reduced ovary weight and oocyte numbers.
- Oocyte quality was significantly impaired, with decreased polar body extrusion and fertilization rates.
- FE disrupted cytoskeletal integrity, induced mitochondrial dysfunction, increased ROS, apoptosis, and autophagy, and altered histone methylation patterns (H3K27me3, H3K9me2) in oocytes.
Conclusions:
- Fenoxaprop-ethyl (FE) adversely affects oocyte quality and fertilization potential in mice.
- Observed effects are attributed to disrupted cytoskeletal integrity and mitochondrial dysfunction, resulting in oxidative stress, apoptosis, and autophagy.
- Epigenetic changes may also contribute to FE-induced reproductive toxicity.
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