Cytoplasmic Component

The degree to which cytoplasmic abnormalities, probably being the result of an impaired cytoplasmic maturation, influence fertilizability and further developmental potential is still a matter of debate (29-33). According to Van Blerkom and Henry (34), the further fate of female gametes is dependent on the first occurrence of certain ooplasmic anomalies, e.g., those developing early in maturation may be associated with failed fertilization and aneu-ploidy while those occurring later in maturation may express developmental failure despite normal fertilization. However, summarizing the relevant literature dealing with cytoplasmic abnormalities, one may conclude that only few cytoplasmic dysmorphisms actually impair viability of the resultant embryo (29,31,33).

On the one hand, aggregation of the smooth endoplasmic reticulum (sER) was shown to significantly reduce rates of implantation and clinical pregnancy (34), even if transferred embryos did not derive from sER aggregation positive ova, which is presumed to be the result of an underlying adverse factor that might have affected the entire follicular cohort (34). Only one pregnancy went to term after transfer of an embryo developed from an affected gamete (34), and to make matters worse, this baby was diagnosed with Beckwith-Wiedemann syndrome.

On the other hand, vacuolization is the most apparent and dynamic cytoplasmic anomaly in human oocytes. Vacuoles are membrane-bound cytoplasmic inclusions filled with fluid virtually identical with perivitelline fluid and they vary in size as well as in number. It is assumed that vacuoles arise either spontaneously (35) or by fusion of preexisting vesicles derived from the smooth endoplasmic reticulum and/or Golgi apparatus (36).

Recently, a prospective analysis revealed that larger vacuoles above a cut-off value (e.g., 14 mm) affect adequate fertilization and severely impair blastocyst development (37). Two hypotheses could explain these phenomena. First, it is likely that a larger vacuole or multiple vacuoles will cause a much more detrimental effect to the oocyte than a small vacuole since a larger portion of the cytoskeleton (e.g., microtubuli) cannot function as supposed to. Secondly, large vacuoles are thought to displace the MII spindle from its polar position which may result in fertilization failure (35).

Regardless of the different types of cytoplasmic inclusions, it has been observed that a deficiency in ooplasmic texture can also reduce reproductive success. Thus, oocytes with impaired fluidity of the cytoplasm, as assessed by the persistence of the injection funnel after ICSI, had a developmental disadvantage compared to MII gametes with regular viscosity (38). However, extensive cytoplasmic granularity is recognized as the most severe form of cytoplasmic texture anomaly since more than half of affected gametes show chromosomal abnormalities (39), which led to minimal rates of implantation (4.2%) and clinical pregnancy (12.8%).

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