AbstractA major obstacel to the study of mammalian development, and to the practical application of knowledge gained from it in the clinic during therapeuticin vitrofertilisation and embryo transfer (IVF‐ET), is the propensity of embryos to become retarded or arrested during their culturein vitro.The precise developmental cell cycle in which embryos arrest or delay is characteristic for the species and coincides with the earliest period of embryonic gene expression. Much evidence reviewed here implicates free oxygen radicals (FORs) in the process of arrest. Thus, studies on the development of mouse preimplantation embryosin vitrohave shown that (i) FORs are elevatedin vitro, but notin vivo, at the time at which embryos become arrested or delayed, (ii) systems for removing reactive oxygen species to limit the formation of hydroxy radicals are present, although they have not yet been assessed quantitatively and may differ qualitatively from those in adult cells, (iii) metabolic and possibly genetic adaptations to oxidative damage are evident, (iv) published procedures for overcomingin vitroarrest are explicable in terms of FOR‐mediated damage or responses and (v) the arrest or delay of most embryosin vitrocan be reduced or prevented experimentally by addition of metal chelators to limit hydroxy radical formation and lipid hydroperoxidat