INTRODUCTION Oocyte cryopreservation provides greater flexibility in breeding programs than embryo cryopreservation (Payner and Fuller, 2007). However, mammalian oocytes are much more readily damaged by cryopreservation than mammalian embryos (Coticchio et al., 2007; Gardner et al., 2007). Differences in plasma membrane permeability to water and cryoprotectants (CPAs) could account for this damage, as could the idiosyncratic physiology of the oocyte itself (Gardner et al., 2007). It is common knowledge that, compared with immature oocytes, the in vivo or in vitro matured oocytes are the preferred stage because of their superior cryotolerance (Otoi et al., 1995; Rojas et al., 2004). However, the meiotic spindles of the matured oocytes are markedly affected by the exposure to CPAs, cooling, and freezing (Van der Elst et al., 1992; Tharasanit et al., 2006; Gardner et al., 2007; Ledda et al., 2007; Mugnusson et al., 2007); exposure to the aforementioned conditions results in an increase in spindle abnormalities and aneuploidy (Pickering et al., 1990; Stachecki et al., 2006; Wu et al., 2006). To avoid this problem, and until suitable protocols for in vitro maturation are available, cryopreservation of immature oocytes is more appropriate (Van der Elst et al., 1992; Agca et al., 1998); immature stage (GV stage) oocytes have a nuclear envelope to protect the nuclear DNA (Hunter and Polge, 1966).