Background: Fenoxaprop-ethyl (FE) is an active ingredient of commercially available herbicide formulations. Its overuse has caused much damage to the environment, livestock breeding, agricultural crops and humans. However, little is known about the effects of FE exposure on female reproductive health and the mechanisms underlying those effects. In this study, we investigated the toxic effects of FE on oocyte quality and their underlying mechanisms in mice fed a diet containing FE.
Results: Ovary weight and numbers of oocytes were reduced in FE-treated mice. Moreover, oocyte quality was seriously impaired, as shown by the reduced rate of first polar body extrusion and fertilization ability in vivo. In FE-treated mice, oocytes presented reduced actin expression and abnormal meiotic spindle morphology, which indicate that cytoskeletal integrality is disrupted. Also, FE induced mitochondrial dysfunction, reflected by the accumulation of reactive oxygen species (ROS), apoptosis and autophagy, as revealed by fluorescent staining analysis and real-time polymerase chain reaction (qPCR). Finally, FE led to changes in epigenetic modifications such as histone H3K27me3 and H3K9me2 in oocytes.
Conclusions: Our results indicate that FE has adverse effects on oocyte quality as assessed by maturation and fertilization potential, due to disrupted cytoskeletal integrality, and mitochondrial dysfunction leading to ROS accumulation, apoptosis and autophagy. © 2018 Society of Chemical Industry.
Keywords: cytoskeleton; epigenetic modifications; fenoxaprop-ethyl; mitochondrial dysfunction.
© 2018 Society of Chemical Industry.