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Bernadette Banrezes; Thierry Sainte-Beuve; Eugénie Canon; Richard M Schultz; José Cancela; Jean-Pierre Ozil
Publisher: Public Library of Science (PLoS)
Journal: PLoS ONE
Languages: English
Types: Article
Subjects: Animal Models, Research Article, Molecular Cell Biology, body weight;oxidation-reduction;oxidative phosphorylation;energy metabolism*;mice;multidisciplinary sciences;science and technology, Mouse, alcalinisation, Morphogenesis, Activation Program, fluorescence, Growth Control, phosphorylation oxydative, analyse statistique, Embryology, mammifère, Germ Cells, fécondation, Cellular Types, collecte d'embryon, Biology, Fertilization, Developmental Biology, Biologie du développement, Medicine, Growth Retardation, production d'embryon, pyruvate, Development Biology, pronucleus, Q, R, souris, Model Organisms, Pediatrics, Science, transfert d'embryon, poids corporel
In mammals fertilization triggers a series of Ca(2+) oscillations that not only are essential for events of egg activation but also stimulate oxidative phosphorylation. Little is known, however, about the relationship between quantitative changes in egg metabolism and specific long-term effects in offspring. This study assessed whether post-natal growth is modulated by early transient changes in NAD(P)H and FAD(2+) in zygotes. We report that experimentally manipulating the redox potential of fertilized eggs during the pronuclear (PN) stage affects post-natal body weight. Exogenous pyruvate induces NAD(P)H oxidation and stimulates mitochondrial activity with resulting offspring that are persistently and significantly smaller than controls. Exogenous lactate stimulates NAD(+) reduction and impairs mitochondrial activity, and produces offspring that are smaller than controls at weaning but catch up after weaning. Cytosolic alkalization increases NAD(P)(+) reduction and offspring of normal birth-weight become significantly and persistently larger than controls. These results constitute the first report that post-natal growth rate is ultimately linked to modulation of NAD(P)H and FAD(2+) concentration as early as the PN stage.

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