Journal
REPRODUCTIVE TOXICOLOGY
Volume 29, Issue 2, Pages 198-205Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.reprotox.2009.10.009
Keywords
Cortisol; Dexamethasone; MAP kinase; Oocyte; Maturation; Fertilization; Stress; Glucocorticoid administration
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Funding
- Spanish Ministry of Education and Science [REN 2003-01587, CGL2006-13340/BOS]
- I3P-CSIC programme
- Royal Society Wolfson Research Merit Award
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High levels of glucocorticoids may alter reproduction, but little is known about their direct actions on oocyte maturation, fertilization and subsequent development. Earlier work suggested negative effects of cortisol or dexamethasone on oocyte maturation but differences were noted between animal models. Both glucocorticoids reduce the p34(cdc2)-cyclin B1 complex but it is unknown if other signaling pathways important for meiosis progression are affected. In this study, using sheep oocytes as a model system, we assessed in vitro the effects of increasing concentration of glucocorticoids (0-250 mu M) on oocyte maturation and underlying changes in the MAP kinase pathway, and the ability of oocytes to undergo fertilization and embryo development. Cortisol decreased oocyte maturation but only at the highest concentration, whereas dexamethasone had no effect. Fertilization and cleavage were not affected. On the other hand, both cortisol and dexamethasone inhibited ERK-1/2 activation in a concentration-dependent manner. It thus seems that oocytes can overcome deleterious effects of glucocorticoids during maturation despite the decrease in ERK-1/2 activity, but repercussions in vivo should be further explored. (C) 2009 Elsevier Inc. All rights reserved.
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