Mitochondrial functions on oocytes and preimplantation embryos

Abstract

Oocyte quality has long been considered as a main limiting factor for in vitro fertilization (IVF). In the past decade, extensive observations demonstrated that the mitochondrion plays a vital role in the oocyte cytoplasm, for it can provide adenosine triphosphate (ATP) for fertilization and preimplantation embryo development and also act as stores of intracellular calcium and proapoptotic factors. During the oocyte maturation, mitochondria are characterized by distinct changes of their distribution pattern from being homogeneous to heterogeneous, which is correlated with the cumulus apoptosis. Oocyte quality decreases with the increasing maternal age. Recent studies have shown that low quality oocytes have some age-related dysfunctions, which include the decrease in mitochondrial membrane potential, increase of mitochondrial DNA (mtDNA) damages, chromosomal aneuploidies, the incidence of apoptosis, and changes in mitochondrial gene expression. All these dysfunctions may cause a high level of developmental retardation and arrest of preimplantation embryos. It has been suggested that these mitochondrial changes may arise from excessive reactive oxygen species (ROS) that is closely associated with the oxidative energy production or calcium overload, which may trigger permeability transition pore opening and subsequent apoptosis. Therefore, mitochondria can be seen as signs for oocyte quality evaluation, and it is possible that the oocyte quality can be improved by enhancing the physical function of mitochondria. Here we reviewed recent advances in mitochondrial functions on oocytes.

Cheetah interspecific SCNT followed by embryo aggregation improves in vitro development but not pluripotent gene expression

“…These organelles are involved in cellular metabolism with ATP production, apoptosis, regulation of calcium and cellular aging (Wang et al 2009b), so an inefficient nucleo-cytoplasmic communication for the regulation of mtDNA transcription and replication can lead to failure in embryonic development. At this stage it was possible to confirm that aggregation has occurred as 61% of the compacted morulae were formed by both founder embryos after mitotracker analysis.…”

Maternal age and in vitro culture affect mitochondrial number and function in equine oocytes and embryos

“…Glutathione peroxidase (GPX) and ATP synthase (ATP synthase-coupling factor 6, mitochondrial-like (ATPsynth_F6)) are enzymes involved in balancing the generation and decomposition of ROS (Ufer and Wang 2011) to help prevent ROS levels reaching a point likely to induce oxidative damage. Increased expression of ATP-synth_F6 has been described in oocytes collected from women .35 years, and in embryonic cells during IVP (Wang et al 2009). …”

“…Advancing maternal age and IVP have both been reported to induce alterations in mitochondrial function that can result in mitochondrial damage (Wilding et al 2001;Wang et al 2009). This manifests as a decrease in mtDNA copy number, a reduction in mitochondrial gene expression and an increased production of ROS within embryonic cells (Giritharan et al 2007(Giritharan et al , 2010.…”

Effect of blood plasma collected after adrenocorticotropic hormone administration during the preovulatory period in the sow on oocyte in vitro maturation

“…4 Mitochondria are energy-converting organelles which generate ATP by oxidative phosphorylation [18] and distribute it to areas of high energy requirement. This is crucial for key events such as oocyte maturation, fertilisation and embryo development [19,20]. A relocation of mitochondria occurs as the oocyte matures, as shown in different species [20][21][22][23]; and a disproportional inheritance of mitochondria during early cleavage can result in arrested development [24].…”

“…This is crucial for key events such as oocyte maturation, fertilisation and embryo development [19,20]. A relocation of mitochondria occurs as the oocyte matures, as shown in different species [20][21][22][23]; and a disproportional inheritance of mitochondria during early cleavage can result in arrested development [24]. Therefore, mitochondrial distribution is a reliable marker of cytoplasmic oocyte maturation [25] and embryo quality [24].…”