Mitochondria: Participation to infertility as source of energy and cause of senescence |
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| Institution: | 1. Reproductive Medicine & Medical Cytogenetics, Centre of Obstetrics and Gynecology, Regional University Hospital and School of Medicine. Picardie University Jules Verne, Amiens, France;2. Fertilys Inc., Laval, Québec QC, Canada;3. Andrology unit, ForteBio Laboratory, Dax, France;4. IVF & Genetics Laboratory, LaboMac, Clinique des Iris, Casablanca, Morocco;1. Department of Pharmacy, Peking University People’s Hospital, Beijing 100044, PR China;2. Central Laboratory, Peking University People’s Hospital, Beijing 100044, PR China;3. Department of Pharmacology, School of Basic Medical Sciences, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, PR China;1. Department of Neurology, Xinqiao Hospital, Third Military Medical University, Chongqing 400037, China;2. Department of Cardiology, Kunming General Hospital of Chengdu Military Command, Yunnan, China;3. Department of Neurology, Boston University School of Medicine, 715 Albany Street, C329, Boston, MA 02118, USA;1. Department of Neurosurgery, Xi’an Central Hospital, School of Medicine, Xi’an Jiao Tong University, No. 185 Houzai Gate of North Street, Xi’an 710003, PR China;2. Department of Neurosurgery, Xijing Hospital, Fourth Military Medical University, No. 17 Changle West Road, Xi’an 710032, PR China;1. Dipartimento di Medicina e Scienze della Salute “V. Tiberio”, Università del Molise, via de Sanctis, Campobasso, Italy;2. Centre de Recherche en Biologie de la Reproduction, Département des Sciences Animales, Université Laval, Québec, Canada;1. Center for Pharmacogenomics, Department of Internal Medicine, Washington University School of Medicine, St. Louis, MO, USA |
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| Abstract: | Mitochondria is a powerhouse organelle involved in ATP synthesis, calcium signaling, reactive oxygen species (ROS) by oxidative stress production, cell cycle arrest via apoptosis and sex steroid hormones biosynthesis. Improvement of sperm parameters such as motility, capacitation, acrosome reaction, and oocyte interaction, involve regulation of ROS levels by the mitochondria. In human, the relation between the quantitative level of mitochondrial DNA (mtDNA), oocyte cytoplasm maturation and fertilization potential, is not clear. It has been hypothesized that oocytes without sufficient wild type mtDNA and therefore able to generate ATP, would not normally be ovulated. This is reflected in the low numbers of mtDNA observed in degenerate oocytes obtained through super ovulation protocols during assisted reproductive technology programs. Different theories place mitochondria in a central role of oxidative damage to cells and tissues related to infertility declining and aging. Mitochondria-dependent apoptosis seems to be responsible for the pre and post-natal decline in germ cells, embryo development, implantation failure, and miscarriages. |
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| Keywords: | Mitochondria Reactive oxygen species Fertility potential Reproductive pathology Infertility |
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