Cardiff University | Prifysgol Caerdydd ORCA
Online Research @ Cardiff 
WelshClear Cookie - decide language by browser settings

Mitochondrial function and redox state in mammalian embryos

Dumollard, R., Carroll, J., Duchen, M. R., Campbell, Karen and Swann, Karl 2009. Mitochondrial function and redox state in mammalian embryos. Seminars in Cell and Developmental Biology 20 (3) , pp. 346-353. 10.1016/j.semcdb.2008.12.013

Full text not available from this repository.


Mitochondria play a central and multifaceted role in the mammalian egg and early embryo, contributing to many different aspects of early development. While the contribution of mitochondria to energy production is fundamental, other roles for mitochondria are starting to emerge. Mitochondria are central to intracellular redox metabolism as they produce reactive oxygen species (ROS, the mediators of oxidative stress) and they can generate TCA cycle intermediates and reducing equivalents that are used in antioxidant defence. A high cytosolic lactate dehydrogenase activity coupled with dynamic levels of cytosolic pyruvate is responsible for a very dynamic intracellular redox state in the oocyte and embryo. Mammalian embryos have a low glucose metabolism during the earliest stages of development, as both glycolysis and the pentose phosphate pathway are suppressed. The mitochondrial TCA cycle is therefore the major source of reducing equivalents in the cytosol so that any change in mitochondrial function in the embryo will be reflected in changes in the intracellular redox state. In the mouse, the metabolic substrates used by the oocyte and early embryo each have a different impact on the intracellular redox state. Pyruvate which oxidises the cytosolic redox state, acts as an energetic and redox substrate whereas lactate, which reduces the cytosolic redox state, acts only as a redox substrate. Mammalian early embryos are very sensitive to oxidative stress which can cause permanent developmental arrest before zygotic genome activation and apoptosis in the blastocyst. The oocyte stockpiles antioxidant defence for the early embryo to cope with exogenous and endogenous oxidant insults arising during early development. Mitochondria provide ATP for glutathione (GSH) production during oocyte maturation and also participate in the regeneration of NADPH and GSH during early development. Finally, a number of pathological conditions or environmental insults impair early development by altering mitochondrial function, illustrating the centrality of mitochondrial function in embryo development.

Item Type: Article
Date Type: Publication
Status: Published
Schools: Medicine
Subjects: R Medicine > R Medicine (General)
R Medicine > RG Gynecology and obstetrics
Uncontrolled Keywords: Early embryos; Mitochondria; Anaplerosis; TCA cycle; Redox state; ATP; Oxidative stress
Publisher: Elsevier
ISSN: 1084-9521
Last Modified: 02 May 2019 11:37

Citation Data

Cited 154 times in Scopus. View in Scopus. Powered By Scopus® Data

Actions (repository staff only)

Edit Item Edit Item