Rotenone Disrupts Meiotic Maturation via Inhibition of Mitochondrial Function in Porcine Oocytes

Background: Rotenone is a commonly used insecticidal chemical in agriculture and it is an inhibitor of mitochondrial complex 1. Previous studies have found that rotenone induces the production of reactive oxygen species (ROS) by inhibiting electron transport in the mitochondria of somatic and germ cells. However, there is little precise information on the effects of rotenone exposure in porcine oocytes during in vitro maturation, and the mechanisms underlying these effects have not been determined. Results: : First, we found that the maturation rate and expansion of cumulus cells was significantly reduced in the 3 and 5 μM rotenone-treated groups. Further experiments showed that rotenone treatment induced mitochondrial dysfunction and failure of mitochondrial biogenesis by repressing the levels of PGC1-α and SIRT1 during in vitro maturation of porcine oocytes. In addition, rotenone treatment reduced the ratio of active mitochondria to total mitochondria, increased ROS production, and decreased ATP production. The levels of LC3 and active-caspase 3 were significantly increased by rotenone treatment, indicating that mitochondrial dysfunction induced by rotenone increased mitophagy but eventually led to apoptosis. Conclusions: : Collectively, these results suggest that rotenone interferes with porcine oocyte maturation by inhibiting mitochondrial function.