Mitoquinone shifts energy metabolism to reduce ROS-induced oxeiptosis in female granulosa cells and mouse oocytes

The female reproductive system is quite sensitive to regulation, and external environmental stimuli may cause oxidative stress which in turn may lead to accelerated aging and programmed cell death in female reproductive cells. The aim of this study was to investigate whether or not mitoquinone (MitoQ) could resist ROS-induced apoptosis in human granulosa cells and mouse oocytes. We found that the MitoQ treatment significantly reduced production of reactive oxygen species (ROS) and imbalance in mitochondrial membrane potential. The MitoQ treatment prevented an excessive mitochondrial fragmentation by upregulating Drp1 S637 and decreasing Drp1 S637 phosphorylation. More importantly, MitoQ maintained aerobic respiration and reduced anaerobic respiration by regulating reprogramming of intracellular energy metabolism, which enhanced cellular ATP production. MitoQ effectively reduced the expressions of AIFM1 and PGAM5, key molecules whose expressions were reversed not only in granulosa cells but also in mouse oocytes. Our findings suggest that MitoQ can ameliorate the mitochondrial deterioration caused by ROS and reprogram cellular energy metabolism, providing protection to cells against apoptosis. The presence of MitoQ may help in protecting human germ cells under in vitro culture conditions.

Automated summary

The aim of this study was to investigate the ability of MitoQ to resist ROS-induced apoptosis in human granulosa cells and mouse oocytes. The results showed that MitoQ treatment reduced ROS production, balanced mitochondrial membrane potential, and prevented excessive mitochondrial fragmentation. MitoQ also regulated intracellular energy metabolism and reduced the expressions of AIFM1 and PGAM5.