Melatonin ameliorates the fertilization capacity of oocytes exposed to 17α-ethynylestradiol

Dai, Xinbin; Qiu, Lijun; Gao, Yang; Mu, Yi; Chu, Zhangjie; Du, Lifei; Xiong, Bo

doi:10.1016/j.reprotox.2020.01.004

Cited by 7 publications

(5 citation statements)

References 30 publications

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“…In unfertilized eggs, ZP2 remains intact and lost sperm binding site after fertilization. In the previous studies, we known that ZP2 is cleaved by an oocyte-specific protease in the CGs called ovastacin after fertilization to block polyspermy (Dai et al, 2020). However, if ovastacin is prematurely exocytosed before fertilization, it will cause defects in sperm binding (Xiong et al, 2017).…”

Section: Discussionmentioning

confidence: 99%

2,4‐DCP compromises the fertilization capacity of mouse oocytes

Dai

Qiu

Rashida

et al. 2021

Journal Cellular Physiology

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Section: Discussionmentioning

confidence: 99%

2,4‐DCP compromises the fertilization capacity of mouse oocytes

Dai

Qiu

Rashida

et al. 2021

Journal Cellular Physiology

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“…The distribution patterns mitochondria and CGs are two well‐accepted indexes for assessing the oocyte cytoplasmic maturation 35 . Our data demonstrated that VAME supplementation recovered the cytoplasmic maturation of LPS‐exposed oocytes by maintaining the normal distribution and function of mitochondria in oocytes, which might be critical for the generation of energy for oocyte development 36,37 . Furthermore, we evidenced that VAME supplementation also advanced the cytoplasmic maturation of LPS‐exposed oocytes by restoring the dynamics of CGs and their component ovastacin.…”

Section: Discussionmentioning

confidence: 52%

“…35 Our data demonstrated that VAME supplementation recovered the cytoplasmic maturation of LPS-exposed oocytes by maintaining the normal distribution and function of mitochondria in oocytes, which might be critical for the generation of energy for oocyte development. 36,37 Furthermore, we evidenced that VAME supplementation also advanced the cytoplasmic maturation of LPS-exposed oocytes by restoring the dynamics of CGs and their component ovastacin. As a component of CGs, ovastacin could destroy the sperm binding site in the zona pellucida of oocytes by cleaving the N-terminal domain of ZP2 to prevent post-fertilization polyspermy.…”

Section: Discussionmentioning

confidence: 78%

Velvet antler water extract protects porcine oocytes from lipopolysaccharide‐induced meiotic defects

et al. 2023

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Previous studies have demonstrated that lipopolysaccharide (LPS), as a central toxic factor of gram-negative bacteria, can induce oxidative stress and cellular inflammation to result in the impairment of female fertility in different organisms. Particularly, it has harmful effects on the oocyte quality and subsequent embryonic development.However, the approach concerning how to prevent oocytes from LPS-induced deterioration still remains largely unexplored. We assessed the effective influences of velvet antler water extract (VAWE) by immunostaining and fluorescence intensity quantification on the meiotic maturation, mitochondrial function and sperm binding ability of oocytes under oxidative stress. Here, we report that VAWE treatment restores the quality of porcine oocytes exposed to LPS. Specifically, LPS exposure contributed to the failed oocyte maturation, reduced sperm binding ability and fertilization capability by disturbing the dynamics and arrangement of meiotic apparatuses and organelles, including spindle assembly, chromosome alignment, actin polymerization, mitochondrial dynamics and cortical granule distribution, the indicators of oocyte nuclear and cytoplasmic maturation. Notably, VAWE treatment recovered these meiotic defects by removing the LPS-induced excessive ROS and thus inhibiting the apoptosis. Collectively, our study illustrates that VAWE treatment is a feasible strategy to improve the oocyte quality deteriorated by the LPS-induced oxidative stress. | INTRODUCTIONGram-negative bacteria possess an outer protective cell wall that harbours several pathogen-associated molecular patterns (PAMPs) to trigger the inflammation and cause other toxic effects when they infect a host or are lysed by antibiotics. 1 Lipopolysaccharide (LPS), as a core component of the outer membrane of gram-negative bacteria, exists extensively in numerous industrial and external environments, including livestock farms, lumbermills and cotton mills. 2,3 LPS is a prototypical PAMP which is identified by toll-like receptor 4 (TLR-4) protein in complex with CD14 and soluble myeloid differentiation factor 2 (MD2) on the cell surface. 4,5 After LPS binds to its receptor, inflammatory molecules such as chemokines IL-8, TNF-α, IL-6 and cytokines IL-1β are released. 4 The LPS-induced molecules cause severe pathology by exerting profound regulatory effects on the cellular functions. 6 In addition, many studies have validated the adverse influences of LPS on the folliculogenesis, oocyte development, ovulation, luteal function, ovarian steroidogenesis, estrus behaviour, and puberty onset in female animals. 7 Notably, a recent study has found that exposure to LPS destructed the oocyte meiotic maturation due

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“…However, negative effects of hormones on oogenesis have been reported. For example, 17α-ethynylestradiol (EE2) can reduce the abundance of Juno protein and increase ROS levels to promote oocyte apoptosis, which can be inhibited by melatonin (Dai et al, 2020).…”

Section: Pharmaceuticalsmentioning

confidence: 99%

Fertility loss: negative effects of environmental toxicants on oogenesis

et al. 2023

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There has been a global decline in fertility rates, with ovulatory disorders emerging as the leading cause, contributing to a global lifetime infertility prevalence of 17.5%. Formation of the primordial follicle pool during early and further development of oocytes after puberty is crucial in determining female fertility and reproductive quality. However, the increasing exposure to environmental toxins (through occupational exposure and ubiquitous chemicals) in daily life is a growing concern; these toxins have been identified as significant risk factors for oogenesis in women. In light of this concern, this review aims to enhance our understanding of female reproductive system diseases and their implications. Specifically, we summarized and categorized the environmental toxins that can affect oogenesis. Here, we provide an overview of oogenesis, highlighting specific stages that may be susceptible to the influence of environmental toxins. Furthermore, we discuss the genetic and molecular mechanisms by which various environmental toxins, including metals, cigarette smoke, and agricultural and industrial toxins, affect female oogenesis. Raising awareness about the potential risks associated with toxin exposure is crucial. However, further research is needed to fully comprehend the mechanisms underlying these effects, including the identification of biomarkers to assess exposure levels and predict reproductive outcomes. By providing a comprehensive overview, this review aims to contribute to a better understanding of the impact of environmental toxins on female oogenesis and guide future research in this field.

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Melatonin ameliorates the fertilization capacity of oocytes exposed to 17α-ethynylestradiol

Cited by 7 publications

References 30 publications

2,4‐DCP compromises the fertilization capacity of mouse oocytes

2,4‐DCP compromises the fertilization capacity of mouse oocytes

Velvet antler water extract protects porcine oocytes from lipopolysaccharide‐induced meiotic defects

Fertility loss: negative effects of environmental toxicants on oogenesis

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