Research Paper Volume 15, Issue 1 pp 246—260
Mitoquinone shifts energy metabolism to reduce ROS-induced oxeiptosis in female granulosa cells and mouse oocytes
- 1 Department of Obstetrics and Gynaecology, Kaohsiung Veterans General Hospital, Kaohsiung 813, Taiwan
- 2 Institute of Biopharmaceutical Sciences, National Sun Yat-Sen University, Kaohsiung 804, Taiwan
- 3 Department of Obstetrics and Gynaecology, National Yang-Ming University School of Medicine, Taipei 112, Taiwan
- 4 Department of Obstetrics and Gynecology, Taipei Veterans General Hospital, Taipei 112, Taiwan
- 5 Department of Pharmacy and Master Program, College of Pharmacy and Health Care, Tajen University, Pingtung County 907, Taiwan
- 6 Department of Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei 114, Taiwan
- 7 College of Health and Nursing, Meiho University, Pingtung County 912, Taiwan
Received: August 30, 2022 Accepted: December 16, 2022 Published: January 9, 2023
https://doi.org/10.18632/aging.204475How to Cite
Copyright: © 2023 Tsui and Li. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
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.