Abstract
Mitochondrial quality control is important for maintaining cellular and oocyte viability. In addition, aging affects mitochondrial quality in many cell types. In the present study, we examined how aging affects oocyte mitochondrial biogenesis and degeneration in response to induced mitochondrial dysfunction. Cumulus oocyte complexes were harvested from the ovaries of young (21‒45 months) and aged (≥120 months) cows and treated for 2 hours with 10 μM carbonyl cyanide-m- chlorophenylhydrazone (CCCP), or a vehicle control, after which cumulus oocyte complexes were subjected to in vitro fertilization and culture. CCCP treatment reduced ATP content and increased reactive oxygen species (ROS) levels in the oocytes of both young and aged cows. When CCCP-treated cumulus oocyte complexes were subsequently cultured for 19 hours and/or subjected to fertilization, high ROS levels in oocytes and a low rate of blastocyst development was observed in oocytes derived from aged cows. In addition, we observed differential responses in mitochondrial biogenesis to CCCP treatment between young and aged cows. CCCP treatment enhanced mitochondrial biogenesis concomitant with upregulation of SIRT1 expression in oocytes of young, but not aged, cows. In conclusion, aging affects mitochondrial quality control and recuperation of oocytes following CCCP-induced mitochondrial dysfunction.
Highlights
Mitochondria are master regulators of energy generation and play versatile roles in apoptosis, calcium storage, and hormone synthesis [1]
In accordance with these findings, we previously reported that oocytes derived from aged cows exhibit high reactive oxygen species (ROS) levels, with decreased mitochondrial DNA (MtDNA) copy number and developmental ability [15,16,17]
carbonyl cyanide-m-chlorophenylhydrazone (CCCP) treatment did not affect the developmental rate of oocytes derived from young cows, but it significantly reduced the developmental ability of oocytes derived from aged cows
Summary
Mitochondria are master regulators of energy generation and play versatile roles in apoptosis, calcium storage, and hormone synthesis [1]. Treatment with CCCP reduces ATP content, increases the expression of sirtuin 1 (SIRT1) and phosphorylated AMP activated protein kinase (pAMPK), and induces mitochondrial generation and degeneration in oocytes, as determined by the kinetics of the MtDNA copy number dynamics, the activation of TFAM expression, and mitophagy markers [23]. On the basis these findings, we suggest that dysfunctional mitochondria may enhance SIRT1 and AMPK activity as well as mitochondrial replenishment through de novo synthesis and degeneration in oocytes. Our study provides additional insights into the role of ageassociated deterioration of mitochondrial quality-control systems is present in bovine oocytes
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