Oxygen consumption by the mouse blastocyst at activation for implantation.

When activated from delayed implantation by an oestrogen injection, mouse blastocysts rapidly increase their oxygen consumption and degree of cytochrome oxidase staining. In the present study, oxygen consumption was augmented to a similar extent also in vitro using a culture system known to permit trophoblast outgrowth. To see whether the increase of oxidative phosphorylation needs the synthesis of new protein or just activation of enzyme precursors, different anti-metabolites were added to the cultures. Inhibitors of transcription (cytosine arabinoside and alpha-amanitin) and RNA translation in the mitochondria (chloramphenicol) were all without effect, whereas blocking cytoplasmic translation by cycloheximide inhibited the increase in oxygen consumption after blastocyst culture. The results suggest that the trophoblast control of oxidative phosphorylation lies post-transcriptionally, and that activation of oxygen consumption involves translation of preformed RNA templates in the cytoplasm.