Evaluation Of Mitochondrial Copy Number Deletions And Mutations As Markers Of Oocyte Competence

Accumulation of mtDNA mutations in the mitochondrial genome may be inherent in oocytes and in embryos derived from them, especially those derived using IVP (see above), and could contribute to impaired metabolic function and thus to developmental incompetence (Keefe et al., 1995; Brenner et al., 1998; Barritt et al., 1999, 2000). Mutations may result in diminished ATP content, leading to defects such as slow or arrested cell division, apoptosis, numerical chromosomal abnormalities such as aneuploidy, and ultimately failure to develop or establish pregnancy (Barnett et al., 1997; Van Blerkom et al., 1995, 2001). But any adverse affect of mtDNA mutations associated with respiratory function would depend upon the magnitude of the mutant population (mutant load). This load could increase with each embryo cell division. Functional defects could also result from asymmetrical mitochondrial distribution following cell division, which could lead to disproportionate mitochondrial inheritance and perhaps thereby produce cells with diminished ATP-generating capacity. This type of error could be related to mitochondrial distribution in the cell (see Migration of Mitochondria in Oocytes and Embryos) (Van Blerkom et al., 1995, 2000). Mitochondria are not only the major site of ATP production in cells but also an important source of reactive oxygen species (ROS) under certain pathological conditions. Because mitochondrial DNA (mtDNA) in the mitochondrial matrix is exposed to ROS that leak from the respiratory chain, this extranuclear genome is prone to mutations. Therefore, the mitochondrial genome is a rich site for both deletions and mutations.

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