Babayev, E., & Seli, E. (2015). Oocyte mitochondrial function and reproduction. Current opinion in obstetrics & gynecology. https://doi.org/10.1097/GCO.0000000000000164
Babayev E, Seli E. Oocyte mitochondrial function and reproduction. Current opinion in obstetrics & gynecology. 2015. doi:10.1097/GCO.0000000000000164
Babayev, Elnur, and Emre Seli. "Oocyte mitochondrial function and reproduction." Current opinion in obstetrics & gynecology, 2015.
Oocyte mitochondria support fertilization and embryo development
Mitochondria in the egg supply the energy that fertilization and early embryo growth need. This 2015 review gathers animal and human studies on how age, diabetes, and IVF laboratory steps relate to egg mitochondria. The authors also describe supplements and mitochondrial replacement.
Key Findings
A fully grown human egg holds about 100 000 mitochondria. Mitochondrial replication is suppressed in the early embryo, so the egg's own mitochondria are the major source of ATP before implantation.
In human eggs, unfertilized oocytes had lower mtDNA copy number, and degenerated oocytes had even lower levels. Higher ATP levels in oocytes correlated with better embryo development and implantation rates.
In 39 healthy mother-child pairs, the number of heteroplasmies in children correlated positively with maternal age at conception. One in eight individuals carries disease-associated heteroplasmy.
Oocytes from diabetic mice, and from mice on a high-fat diet, showed altered mitochondria and more spindle abnormalities. Ovarian hyperstimulation lowered mitochondrial copy number, membrane potential and ATP content in murine oocytes.
Transfer of cytoplasm from young oocytes into the oocytes of women with repeated IVF failures was discontinued over concern about heteroplasmy and the long-term health of offspring.
Interpretation
This 2015 review examined animal and human studies on egg mitochondria. Mitochondria affect fertilization and early embryo growth. The authors say the link between egg mitochondrial DNA and embryo potential needs more study. They call for larger clinical studies of mitochondrial nutrients and mitochondrial replacement.
RRM Context
Restorative reproductive medicine investigates why egg quality is poor. The review reports egg mitochondrial changes with age, and with diabetes and a high-fat diet in mice. Its mouse data on ovarian hyperstimulation give a biological rationale for care that works with the natural cycle.
Our editorial summary of this paper, not the article's abstract.
Abstract
Purpose of Review
Mitochondria are cellular organelles that are required for energy production. Emerging evidence demonstrates their role in oocyte development and reproduction. In this review, we examine recent animal and clinical studies on the role of mitochondria in fertility. We also analyse the impact of assisted reproductive techniques (ARTs) on mitochondrial function and discuss the future clinical implications of mitochondrial nutrients and mitochondrial replacement.
Recent Findings
Mitochondria affect all aspects of mammalian reproduction. They are essential for optimal oocyte maturation, fertilization and embryonic development. Mitochondrial dysfunction causes a decrease in oocyte quality and interferes with embryonic development. ART procedures affect mitochondrial function, while mitochondrial nutrients may increase mitochondrial performance in oocytes. New mitochondrial replacement procedures using mitochondria obtained from polar bodies or from the patient's own oogonial stem cells are promising and may address concerns related to the induction of high-levels of heteroplasmy, which could potentially result in negative long-term health effects.
Summary
Optimal energy production is required for oocyte and embryo development, and mitochondrial abnormalities have devastating reproductive consequences. Improvement of oocyte mitochondrial function via intake of compounds that boost mitochondrial activity may have clinical benefits, and mitochondrial replacement could potentially be used for the prevention of mitochondrial diseases.
03v76x132 