Restraint stress of female mice during oocyte development facilitates oocyte postovulatory aging

Abstract

Studies suggest that psychological stress on women can impair their reproduction and that postovulatory oocyte aging (POA) might increase the risk of early pregnancy loss and affect offspring's reproductive fitness and longevity. However, whether psychological stress during oocyte development would facilitate POA is unknown but worth exploring to understand the mechanisms by which psychological stress and POA damage oocytes. This study observed effects of female restraint stress during oocyte development (FRSOD) on oocyte resistance to POA. Female mice were restrained for 48 h before superovulation, and they were sacrificed at different intervals after ovulation to recover aging oocytes for analyzing their early and late aged characteristics. The effects of FRSOD on aging oocytes included: (1) increasing their susceptibility to activation stimulus with elevated cytoplasmic calcium; (2) impairing their developmental potential with downregulated expression of development-beneficial genes; (3) facilitating degeneration, cytoplasmic fragmentation and apoptosis; (4) worsening the disorganization of cortical granules and spindle/chromosomes; and (5) impairing redox potential with increased oxidative stress. In conclusion, FRSOD impairs oocyte resistance to POA, so that stressed oocytes become aged significantly quicker than unstressed controls. Thus, couples wishing to achieve pregnancy should take steps to avoid not only fertilization of aged oocytes but also pregestational stressful life events.

The effect of norepinephrine on ovarian dysfunction by mediating ferroptosis in mice model

“…In animal experiments, chronic stress has been shown to disrupt the estrous cycle, alter hormone levels, and decrease follicle numbers in mice [10,11]. Stress can also induce cytoplasmic fragmentation, apoptosis, spindle disorders, and oxidative stress, accelerating the aging of mouse oocytes and increasing the risk of early pregnancy failure [12].…”

Role of calcium-sensing receptor in regulating activation susceptibility of postovulatory aging mouse oocytes

“…However, the mechanisms underlying increased STAS levels in aging oocytes are largely unclear. Kong et al [11] and Chen et al [12] have reported that cytoplasmic calcium is correlated with STAS in aging mouse oocytes. Cui et al [13] observed that cytoplasmic Ca 2+ levels were increased in rat oocytes undergoing spontaneous activation during postovulatory aging.…”