Shifts in Atp Synthesis During Preimplantation Stages of Mouse Embryos

Abstract

The actual and potential activities of the cyochrome system were studied in cleavage-stage mouse embroys. Activities were determined by assaying embroys for total ATP and the rates of [32-P]ATP synthesis both before and after their incubation in medium supplemented either with an energy coupling site inhibitor (antimycin, amytal or cyanide) or with the FADH-linked substrate, succinate. The data indicate that there are three major shifts in the mode of ATP production during preimplantation stages: the first, between the two-cell and late four-cell stages; the second, between the eight-celland late morula stages; and the third, between the late morula and late blastocyst stages. These data are discussed in relation to studies on the energy metabolism of cleavage and blastocyst stage mouse embryos.

Oxidative Phosphorylation-Dependent and -Independent Oxygen Consumption by Individual Preimplantation Mouse Embryos1

“…Although the estimations of OXPHOS-dependent/OX-PHOS-independent ratios are based upon pharmacological manipulations, and therefore should be interpreted with caution, they are consistent with a host of other related changes that occur during preimplantation embryo development including: changes in mitochondria morphology from condensed structures in cleavage-stage embryos to swollen cristae-containing organelles in blastocysts [42][43][44][45][46][47]; an increase in mitochondria number in blastocysts resulting from mitochondria DNA and structural replication [44][45][46][47][48][49]; changes in the biogenesis of key OXPHOS enzymes [50,51]; a decrease in total ATP content and ATP/ ADPϩP ratio that would stimulate OXPHOS [35,52,53]; and a change in energy substrate preferences and waste product secretion [18, 24, 25, 34-36, 54, 55].…”

Mitochondria in human oogenesis and preimplantation embryogenesis: engines of metabolism, ionic regulation and developmental competence

“…Many studies, some beginning in the 1930s (Boeil & Nicholas 1939) and continuing during the subsequent decades (Fridhandler 1961, Brinster 1967, Stern et al 1971, Ginsberg & Hillman 1973, 1975a, Biggers & Borland 1976, Gott et al 1990 up to the present time (for review see Biggers 2004), have examined metabolic pathways of ATP generation during early mammalian embryogenesis. It is clear that mitochondrial oxidative metabolism is a major contributor of ATP during the entire preimplantation stage, with over 85 % of all ATP produced in the mouse blastocyst derived from mitochondria (Benos & Balaban 1983).…”

“…Early cleavage arrest in the homozygous embryos of certain mutant mouse strains (Ginsberg & Hillman 1975b) has been related to unusually high levels of mitochondrial oxidative phosphorylation and correspondingly high cytoplasmic ATP levels. A situation where mitochondrial ATP supply exceeds cellular demand could be toxic if associated with elevated levels of oxidative free radical production which could cause irreversible nuclear and mtDNA damage leading to cytoplasmic deterioration, mitochondrial disruption and eventually death by degenerative or apoptotic processes .…”

The modifier ofMin2 (Mom2) locus: Embryonic lethality of a mutation in theAtp5a1gene suggests a novel mechanism of polyp suppression

“…Anoxic respiration is the primary form of ATP production until implantation and the formation of the placenta (Houghton et al 1996). Aerobic respiration increases during late blastocyst stage (Ginsberg and Hillman 1975). With the increasing demands for aerobic respiration and energy needs during blastocoel formation and implantation, it is likely that the homozygous Mom2 R embryos die around this stage of development due to their inability to produce sufficient energy for their needs.…”