ATP is critical for oocyte maturation, fertilization, and subsequent embryo development.
Both mitochondrial membrane potential and copy number expand during oocyte maturation. In
order to differentiate the roles of mitochondrial metabolic activity and mtDNA copy number
during oocyte maturation, we used two inhibitors, FCCP (carbonyl cyanide
p-(tri-fluromethoxy)phenyl-hydrazone) and ddC (2’3-dideoxycytidine), to deplete the
mitochondrial membrane potential (Δφm) and mitochondrial copy number,
respectively. FCCP (2000 nM) reduced ATP production by affecting mitochondrial
Δφm, decreased the mRNA expression of Bmp15 (bone
morphogenetic protein 15), and shortened the poly(A) tails of Bmp15,
Gdf9 (growth differentiation factor 9), and Cyclin B1
transcripts. FCCP (200 and 2000 nM) also affected p34cdc2 kinase activity. By
contrast, ddC did not alter ATP production. Instead, ddC significantly decreased mtDNA
copy number (P < 0.05). FCCP (200 and 2000 nM) also decreased extrusion of the first
polar body, whereas ddC at all concentrations did not affect the ability of immature
oocytes to reach metaphase II. Both FCCP (200 and 2000 nM) and ddC (200 and 2000 µM)
reduced parthenogenetic blastocyst formation compared with untreated oocytes. However,
these inhibitors did not affect total cell number and apoptosis. These findings suggest
that mitochondrial metabolic activity is critical for oocyte maturation and that both
mitochondrial metabolic activity and replication contribute to the developmental
competence of porcine oocytes.