Coenzyme Q10 restores oocyte mitochondrial function and fertility during reproductive aging

Assaf Ben-Meir, Eliezer Burstein, Aluet Borrego-Alvarez, Jasmine Chong, Ellen Wong, Tetyana Yavorska, Taline Naranian, Maggie Chi, Ying Wang, Yaakov Bentov, Jennifer Alexis, James Meriano, Hoon Ki Sung, David L. Gasser, Kelle H. Moley, Siegfried Hekimi, Robert F. Casper, Andrea Jurisicova

Research output: Contribution to journalArticlepeer-review

204 Scopus citations

Abstract

Female reproductive capacity declines dramatically in the fourth decade of life as a result of an age-related decrease in oocyte quality and quantity. The primary causes of reproductive aging and the molecular factors responsible for decreased oocyte quality remain elusive. Here, we show that aging of the female germ line is accompanied by mitochondrial dysfunction associated with decreased oxidative phosphorylation and reduced Adenosine tri-phosphate (ATP) level. Diminished expression of the enzymes responsible for CoQ production, Pdss2 and Coq6, was observed in oocytes of older females in both mouse and human. The age-related decline in oocyte quality and quantity could be reversed by the administration of CoQ10. Oocyte-specific disruption of Pdss2 recapitulated many of the mitochondrial and reproductive phenotypes observed in the old females including reduced ATP production and increased meiotic spindle abnormalities, resulting in infertility. Ovarian reserve in the oocyte-specific Pdss2-deficient animals was diminished, leading to premature ovarian failure which could be prevented by maternal dietary administration of CoQ10. We conclude that impaired mitochondrial performance created by suboptimal CoQ10 availability can drive age-associated oocyte deficits causing infertility.

Original languageEnglish
Pages (from-to)887-895
Number of pages9
JournalAging Cell
Volume14
Issue number5
DOIs
StatePublished - Oct 1 2015

Keywords

  • Anti-aging
  • Fecundity
  • Individual
  • Mitochondria
  • Molecular biology of aging
  • Mouse models

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