Alterations in the rate of oocyte meiotic maturation (OM) and the timing ofthe metaphase-anaphase transition may predispose oocytes to prematurecentromere separation (PCS) and aneuploidy. Tamoxifen has the potential forperturbing the rate of OM since it can function as a calcium antagonist bybinding to calmodulin and inhibiting the formation of a calcium-calmodulincomplex which is needed for activating calmodulin-dependent cAMPphosphodiesterase and initiating OM. The objective of this study was totest the hypothesis that tamoxifen alters the rate of OM and predisposesoocytes to PCS and aneuploidy. Different does of tamoxifen were administeredby oral gavage to female mice preovulation. Metaphase II oocyte and 1-cellzygote chromosomes were C-banded and cytogenetically analysed. Tamoxifentreatment resulted in a modest, but significant (p < 0.05), increase inoocytes with PCS. Similar frequencies of hyperploidy and oocytes withunpaired, single chromatids (SC) were found. Metaphase I, diploid andpremature anaphase (PA) oocytes were not detected. Hyperploidy, polyploidy,PCS, PA and SC were not detected in zygotes. These data indicate that thelevels of tamoxifen-induced PCS found in mouse oocytes did not predisposezygotes to aneuploidy. Tamoxifen did, however, reduce the proportion offemales exhibiting oestrus.