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Association of female aging with decreased parthenogenetic activation, raised MPF, and MAPKs activities and reduced levels of glutathione S‐transferases activity and thiols in mouse oocytes
Author(s) -
Tarín Juan J.,
GómezPiquer Vanessa,
Pertusa José F.,
Hermenegildo Carlos,
Cano Antonio
Publication year - 2004
Publication title -
molecular reproduction and development
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.745
H-Index - 105
eISSN - 1098-2795
pISSN - 1040-452X
DOI - 10.1002/mrd.20180
Subject(s) - dithiothreitol , biology , glutathione , parthenogenesis , medicine , endocrinology , andrology , gonadotropin , biochemistry , embryo , microbiology and biotechnology , enzyme , hormone
This study aims to determine in the mouse whether oocytes from reproductively old females exhibit a different susceptibility to be parthenogenetically activated when compared to oocytes from young females. At the age of 10–12 (young‐female group) or 60–62 (old‐female group) weeks, hybrid female mice were superovulated using pregnant mare's serum gonadotropin (PMSG) followed by human chorionic gonadotropin (hCG) 48 hr later. After removing the cumulus cells, oocytes were exposed to any of two different activating protocols: (a) 6‐min exposure to 8% ethanol; and (b) treatment with 200 μM thimerosal for 15 min followed by 8 mM dithiothreitol (DTT) for 30 min. Oocytes from old female mice displayed (1) lower total percentage of parthenogenetic activation and extrusion of the second polar body after treatment with either thimerosal + DTT or ethanol; (2) higher M‐phase‐promoting factor (MPF) and mitogen‐activated protein kinases (MAPKs) activities; and (3) lower intracytoplasmic levels of glutathione S‐transferases (GSTs) activity and thiols than oocytes from young females. These data show that female aging is associated with higher resistance of oocytes to be parthenogenetically activated, higher MPF and MAPKs activities and lower intracytoplasmic levels of GSTs activity and thiols. Mol. Reprod. Dev. 69: 402–410, 2004. © 2004 Wiley‐Liss, Inc.