A Nuclear and Cytoplasmic Characterization of Bovine Oocytes Reveals That Cysteamine Partially Rescues the Embryo Development in a Model of Low Ovarian Reserve.

Valentina Lodde,David F Albertini,Federica Franciosi,Ileana Miclea,Irene Tessaro,Giulia Musmeci,Alberto Maria Luciano,Mariella Aru

doi:10.3390/ani11071936

Valentina Lodde, David F Albertini + Show 6 more

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Decreased oocyte quality is a major determinant of age-associated fertility decline. Similarly, individuals affected by early ovarian aging carry low-quality oocytes. Using an established bovine model of early ovarian aging, we investigated key features of 'quality' oocyte maturation, associated with the onset of egg aneuploidy and reproductive aging, such as histone modifications, mitochondria distribution and activity, reduced glutathione (GSH) content, and gap junction functionality. Bovine ovaries were classified according to the antral follicle count (AFC), and the retrieved oocytes were processed immediately or matured in vitro. We observed alterations in several cellular processes, suggesting a multifactorial etiology of the reduced oocyte quality. Furthermore, we performed a rescue experiment for one of the parameters considered. By adding cysteamine to the maturation medium, we experimentally increased the free radical scavenger ability of the 'low competence' oocytes and obtained a higher embryo development. Our findings show that adopting culture conditions that counteract the free radicals has a positive impact on the quality of 'compromised' oocytes. Specifically, cysteamine treatment seems to be a promising option for treating aging-related deficiencies in embryo development.

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With women’s reproductive performance starting to decline in the mid-30s and having extremely small possibilities of becoming pregnant by the age of 40–45 [1,2], female age is one of the most important predictors of reproductive success
Reproductive aging is associated with a higher incidence of errors in the segregation of the chromosomes, leading to aneuploid eggs, which in turn is responsible for embryo and pregnancy loss and genetic anomalies of the offspring (e.g., Down syndrome) [6,7,8,9]
H4K12 by indirect in im-70 fluorescence and quantified theand relative fluorescence munofluorescence (Figures 1 and 2, respectively) and quantified the relative fluorescence oocytes collected from high AFC (Hi) ovaries and 61 oocytes collected from low AFC (Lo) ovaries (Hi- and Loin 70 oocytes collected from Hi ovaries and 61 oocytes collected from Lo ovaries (Hi- and oocyte,Lo-oocyte, respectively) at the GV and metaphase II (MII) stages

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With women’s reproductive performance starting to decline in the mid-30s and having extremely small possibilities of becoming pregnant by the age of 40–45 [1,2], female age is one of the most important predictors of reproductive success. A depletion of the follicle reserve and low oocyte quality are critical factors in this fertility decline, which is referred to as reproductive aging [3,4,5]. A distinctive morphological trait of reproductive aging, used to predict the ovarian reserve, is the observation of few antral follicles on the ovary’s surface, referred to as low antral follicle count (AFC) [10,11]. Besides the decrease in the ovarian reserve and oocyte quality, reproductive aging is associated with a distinctive hormonal profile, characterized by high serum levels of basal follicle-stimulating hormone (FSH) and low anti-Mullerian hormone (AMH) [14,15,16,17,18]

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