SUMMARYOne of the biggest obstacles in the in vitro embryo production for basic research, commercial purposes, or conservation, is the blockade of the early cleavage, which occurs on a species-specific manner in a particular stage of development. To explain this phenomenon some causative factors have been postulated such as: disturbances in chromatin, cytoskeleton rearrangement, oxidative stress and mitochondrial damage. The latter has received considerable attention because mitochondrion is a source of reactive oxygen species (ROS), and oxidative stress is a critical mediator of physiological and pathological states. Over the past years it has been shown that hydrogen peroxide (H 2 O 2 ) is a pivoting molecule able to trigger cell death by different mechanisms that may or may not involve the transcription factors such as NFκB-p53, and is executed by effector caspases. It is believed that mitochondria may play an important role as a producer or as a target of H 2 O 2 , and as a mediator in apoptotic death of embryos. The purpose of this review is to present the state of the art about apoptosis triggered by oxidative stress and mediated by mitochondria in in vitro produced bovine embryos, as part of the explanation for the low efficiency in this process.Palabras clave: apoptosis, NFκB, potencial transmembranal mitocondrial, p53.