title: Developmental potential of prepubertal mouse oocytes is compromised due mainly to their impaired synthesis of glutathione.
abstract: Although oocytes from prepubertal animals are found less competent than oocytes from adults, the underlying mechanisms are poorly understood. Using the mouse oocyte model, this paper has tested the hypothesis that the developmental potential of prepubertal oocytes is compromised due mainly to their impaired potential for glutathione synthesis. Oocytes from prepubertal and adult mice, primed with or without eCG, were matured in vitro and assessed for glutathione synthesis potential, oxidative stress, Ca(2+) reserves, fertilization and in vitro development potential. In unprimed mice, abilities for glutathione synthesis, activation, male pronuclear formation, blastocyst formation, cortical granule migration and polyspermic block were all compromised significantly in prepubertal compared to adult oocytes. Cysteamine and cystine supplementation to maturation medium significantly promoted oocyte glutathione synthesis and blastocyst development but difference due to maternal age remained. Whereas reactive oxygen species (ROS) levels increased, Ca(2+) storage decreased significantly in prepubertal oocytes. Levels of both catalytic and modifier subunits of the γ-glutamylcysteine ligase were significantly lower in prepubertal than in adult oocytes. Maternal eCG priming improved all the parameters and eliminated the age difference. Together, the results have confirmed our hypothesis by showing that prepubertal oocytes have a decreased ability to synthesize glutathione leading to an impaired potential to reduce ROS and to form male pronuclei and blastocysts. The resulting oxidative stress decreases the intracellular Ca(2+) store resulting in impaired activation at fertilization, and damages the microfilament network, which affects cortical granule redistribution leading to polyspermy.
authors.affiliation: College of Animal Science and Veterinary Medicine, Shandong Agricultural University, Tai-an City, People's Republic of China.
authors.forename: Guang-Zhong
authors.initials: GZ
authors.lastname: Jiao
authors.forename: Xin-Yan
authors.initials: XY
authors.lastname: Cao
authors.forename: Wei
authors.initials: W
authors.lastname: Cui
authors.forename: Hua-Yu
authors.initials: HY
authors.lastname: Lian
authors.forename: Yi-Long
authors.initials: YL
authors.lastname: Miao
authors.forename: Xiu-Fen
authors.initials: XF
authors.lastname: Wu
authors.forename: Dong
authors.initials: D
authors.lastname: Han
authors.forename: Jing-He
authors.initials: JH
authors.lastname: Tan
mesh_terms: D000367:Age Factors; D000818:Animals; D001755:Blastocyst / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D002118:Calcium / Q000378:metabolism; D002478:Cells, Cultured; D006063:Chorionic Gonadotropin / Q000494:pharmacology; D003470:Culture Media; D003543:Cysteamine / Q000378:metabolism / Q000494:pharmacology; D003553:Cystine / Q000378:metabolism / Q000494:pharmacology; D004338:Drug Combinations; D046149:Embryo Culture Techniques; D004622:Embryo, Mammalian; D047108:Embryonic Development; D005260:Female; D005307:Fertilization in Vitro; D005978:Glutathione / Q000096:biosynthesis*; D006064:Gonadotropins, Equine / Q000494:pharmacology; D051379:Mice; D009865:Oocytes / Q000166:cytology / Q000187:drug effects / Q000254:growth & development / Q000378:metabolism*; D018384:Oxidative Stress; D017382:Reactive Oxygen Species / Q000378:metabolism; D012741:Sexual Maturation / Q000502:physiology*
chemical_list: D006063:Chorionic Gonadotropin; D003470:Culture Media; D004338:Drug Combinations; D006064:Gonadotropins, Equine; D017382:Reactive Oxygen Species; D003553:Cystine; D003543:Cysteamine; C006116:chorionic gonadotropin, pregnant mare serum gonadotropin drug combination; D005978:Glutathione; D002118:Calcium