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Co-Enzyme Q10 Supplementation Rescues Cumulus Cells Dysfunction in a Maternal Aging Model

Lunenfeld Tanenbaum Research Institute, Mount Sinai Hospital, 25 Orde Street, Toronto, ON M5T 3H7, Canada
TRIO Fertility Partners, 655 Bay St, Suite 1101, Toronto, ON M5G2K4, Canada
Department of Physiology, University of Toronto, 1 King’s College Circle, Toronto, ON M5S 1A8, Canada
Department of Obstetrics and Gynecology, University of Toronto, 92 College Street, Toronto, ON M5G 1L4, Canada
Author to whom correspondence should be addressed.
Current address: Department of Obstetrics and Gynecology, Hadassah-Hebrew University Medical Center, Ein Kerem P.O.B. 12000, Jerusalem 91120, Israel.
Current address: Division of Reproductive Endocrinology and Infertility, Department of OB-GYN, Dartmouth Hitchcock Medical Center, Geisel School of Medicine, Lebanon, NH 03756, USA.
Current address: Juno Fertility, 430 The Boardwalk suite 402, Waterloo, ON N2T 0C1, Canada.
Antioxidants 2019, 8(3), 58;
Received: 26 January 2019 / Revised: 17 February 2019 / Accepted: 1 March 2019 / Published: 8 March 2019
(This article belongs to the Special Issue CoQ10 in Longevity)
PDF [1234 KB, uploaded 8 March 2019]


Over the past four decades, due to cultural and social changes, women in the developed world have significantly delayed childbirth. This trend is even worse for patients who attend infertility clinics. It is well-known that live birth rates in women older than 35 are significantly lower than in those younger, both naturally and with assisted reproduction. Fertility decline is, in part, due to an increase in oocyte aneuploidy that leads to a reduced embryo quality, as well as an increased incidence of miscarriages and birth defects. Here we show that aging-associated malfunction is not restricted to the oocyte, as cumulus granulosa cells also display a series of defects linked to mitochondrial activity. In, both, human and mouse model, a decline in cumulus cell function due to increased maternal age is accompanied by a decreased expression of enzymes responsible for Coenzyme Q (CoQ) production, particularly Pdss2 and CoQ6. In an aged mouse model supplementation with Coenzyme Q10—a potent stimulator of mitochondrial function—restored cumulus cell number, stimulated glucose uptake, and increased progesterone production. CoQ10 supplementation might, thus, improve oocyte and cumulus cells quantity and quality, by improving the mitochondrial metabolism in females of advanced maternal age. View Full-Text
Keywords: aging; cumulus cells; mitochondria; apoptosis aging; cumulus cells; mitochondria; apoptosis

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Ben-Meir, A.; Kim, K.; McQuaid, R.; Esfandiari, N.; Bentov, Y.; Casper, R.F.; Jurisicova, A. Co-Enzyme Q10 Supplementation Rescues Cumulus Cells Dysfunction in a Maternal Aging Model. Antioxidants 2019, 8, 58.

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