Understanding cellular disruptions during early embryo development that perturb viability and fetal development

Abstract

An inability to regulate ionic and metabolic homeostasis is related to a reduction in the developmental capacity of the embryo. The early embryo soon after fertilisation and up until compaction appears to have a reduced capacity to regulate its homeostasis. The reduced ability to regulate homeostasis, such as intracellular pH and calcium levels, by the precompaction-stage embryo appears to impact on the ability to regulate mitochondrial function and maintain adequate levels of energy production. This reduction in ATP production causes a cascade of events leading to disrupted cellular function and, perhaps ultimately, disrupted epigenetic regulation and aberrant placental and fetal development. In contrast, after compaction the embryo takes on a more somatic cell-like physiology and is better able to regulate its physiology and therefore appears less vulnerable to stress. Therefore, for human IVF it would seem important for the establishment of healthy pregnancies that the embryos are maintained in systems that are designed to minimise homeostatic stress, particularly for the cleavage-stage embryos, as exposure to stress is likely to culminate in impaired embryo function.