Chloroacetonitrile exposure induces endoplasmic reticulum stress and affects spindle assembly in mouse oocytes

Chloroacetonitrile (CAN) is a halogenated acetonitrile often produced while disinfecting drinking water. Pre-vious studies have shown that maternal exposure to CAN interferes with fetal development; however, the adverse effects on maternal oocytes remain unknown. In this study, in vitro exposure of mouse oocytes to CAN reduced maturation significantly. Transcriptomics analysis showed that CAN altered the expression of multiple oocyte genes, especially those associated with the protein folding process. CAN exposure induced reactive oxygen species production, accompanied by endoplasmic reticulum (ER) stress and increased glucose regulated protein 78, C/EBP homologous protein and activating transcription factor 6 expression. Moreover, our results indicated that spindle morphology was impaired after CAN exposure. CAN disrupted polo-like kinase 1, pericentrin and p -Aurora A distribution, which may be an origin inducer that disrupts spindle assemble. Furthermore, exposure to CAN in vivo impaired follicular development. Taken together, our findings indicate that CAN exposure induces ER stress and affects spindle assembly in mouse oocytes.

Automated summary

This study found that exposure to chloroacetonitrile (CAN) significantly impairs the maturation of mouse oocytes, alters the expression of multiple oocyte genes, induces reactive oxygen species production, ER stress and affects spindle assembly. In vivo experiments also showed impaired follicular development. These findings suggest that CAN exposure has adverse effects on mouse oocytes.