Abstract
Acquiring oocyte competence requires optimal mitochondrial function and adequate ATP levels. In this context, CoQ10 supplementation may improve human oocyte quality and subsequent reproductive performance given its role in ATP synthesis and mitochondrial protection from ROS oxidative damage. In infertility treatments, CoQ10 therapy can be orally supplied to promote a more favorable environment for oocyte development in vivo or by its addition to culture media in an attempt to improve its quality in vitro. Human clinical studies evaluating the impact of CoQ10 on reproductive performance are summarized in this review, although the available data do not clearly prove its ability to improve human oocyte quality. The main objective is to provide readers with a complete overview of this topic’s current status as well as the keys for potential future research lines that may help to take this therapy to clinical practice. Indeed, further clinical trials are needed to confirm these results along with molecular studies to evaluate the impact of CoQ10 supplementation on oxidative stress status and mitochondrial function in human gametes.
Highlights
Acquiring oocyte competence requires optimal mitochondrial function and adequate ATP levels
Insufficient levels of this molecule are associated with the consumption of some drugs [4], certain diseases in which a mutation in a gene implicated in Coenzyme Q10 (CoQ10) synthesis is involved [5], and advanced age [6]
The decline in human oocyte quality associated with the aging process has been linked with increased oxidative stress and/or mitochondrial dysfunction [7] as mitochondria are necessary for proper meiotic spindle assembly, ijms22179541
Summary
Coenzyme Q10 (CoQ10) is a fat-soluble lipophilic molecule ubiquitously situated in the hydrophobic domain of all cell membranes. Insufficient CoQ10 levels could lead to diminished mitochondrial respiration activity, which may result in lower ATP production, less ROS counteraction, increased oxidative stress, mitochondrial damage, and subsequent mitochondrial dysfunction. The decline in human oocyte quality associated with the aging process has been linked with increased oxidative stress and/or mitochondrial dysfunction [7] as mitochondria are necessary for proper meiotic spindle assembly, ijms22179541. In 2011, Turi’s group analyzed, for the first time, the CoQ10 drial dysfunction [7] as mitochondria are necessary for proper meiotic spindle assembly, levels in the FF of women undergoing infertility treatment Even though they found no dithe chromosomes, maturation, fertilization, and embryo rectsegregation association of between these levels and oocyte/embryo quality [12], in development.
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