Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2013:2013:183024.
doi: 10.1155/2013/183024. Epub 2013 May 16.

The role of mitochondria from mature oocyte to viable blastocyst

Affiliations

The role of mitochondria from mature oocyte to viable blastocyst

Scott Chappel. Obstet Gynecol Int. 2013.

Abstract

The oocyte requires a vast supply of energy after fertilization to support critical events such as spindle formation, chromatid separation, and cell division. Until blastocyst implantation, the developing zygote is dependent on the existing pool of mitochondria. That pool size within each cell decreases with each cell division. Mitochondria obtained from oocytes of women of advanced reproductive age harbor DNA deletions and nucleotide variations that impair function. The combination of lower number and increased frequency of mutations and deletions may result in inadequate mitochondrial activity necessary for continued embryo development and cause pregnancy failure. Previous reports suggested that mitochondrial activity within oocytes may be supplemented by donor cytoplasmic transfer at the time of intracytoplasmic sperm injection (ICSI). Those reports showed success; however, safety concerns arose due to the potential of two distinct populations of mitochondrial genomes in the offspring. Mitochondrial augmentation of oocytes is now reconsidered in light of our current understanding of mitochondrial function and the publication of a number of animal studies. With a better understanding of the role of this organelle in oocytes immediately after fertilization, blastocyst and offspring, mitochondrial augmentation may be reconsidered as a method to improve oocyte quality.

PubMed Disclaimer

References

    1. Koopman WJ, Willems PH, Smeitink JA. Monogenic mitochondrial disorders. The New England Journal of Medicine. 2012;366:1132–1141. - PubMed
    1. Anderson S, Bankier AT, Barrell BG, et al. Sequence and organization of the human mitochondrial genome. Nature. 1981;290:457–465. - PubMed
    1. Jiang Y, Wang X. Comparative mitochondrial proteomics: perspective in human diseases. Journal of Hematology and Oncology. 2012;5, article 11 - PMC - PubMed
    1. Mootha VK, Bunkenborg J, Olsen JV, et al. Integrated analysis of protein composition, tissue diversity, and gene regulation in mouse mitochondria. Cell. 2003;115(5):629–640. - PubMed
    1. Kenyon L, Moraes CT. Expanding the functional human mitochondrial DNA database by the establishment of primate xenomitochondrial cybrids. Proceedings of the National Academy of Sciences of the United States of America. 1997;94(17):9131–9135. - PMC - PubMed