Di (2-ethylhexyl) phthalate impairs primordial follicle assembly by increasing PDE3A expression in oocytes

Liu, Jing-Cai; Yan, Zihui; Li, Bo; Yan, Hong‐Chen; Felici, Massimo De; Shen, Wei

doi:10.1016/j.envpol.2020.116088

Cited by 21 publications

(10 citation statements)

References 48 publications

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“…Studies using single phthalates indicated that exposure to DEHP caused DNA damage, increased oxidative stress, delayed progression of meiotic prophase I, and disrupted homologous recombination in an estrogen-receptor-dependent manner compared to controls in neonatal ovary cultures [ 26 ]. Further, DEHP exposure alone impaired germ cell nest breakdown and impaired primordial follicle assembly compared to controls in neonatal ovary cultures [ 27 , 28 , 29 ].…”

Section: Effects Of Single Phthalate and Phthalate Mixture Exposure O...mentioning

confidence: 99%

Effects of Phthalate Mixtures on Ovarian Folliculogenesis and Steroidogenesis

Fletcher

Santacruz-Márquez

Mourikes

et al. 2022

Toxics

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The female reproductive system is dependent upon the health of the ovaries. The ovaries are responsible for regulating reproduction and endocrine function. Throughout a female’s reproductive lifespan, the ovaries undergo continual structural changes that are crucial for the maturation of ovarian follicles and the production of sex steroid hormones. Phthalates are known to target the ovaries at critical time points and to disrupt normal reproductive function. The US population is constantly exposed to measurable levels of phthalates. Phthalates can also pass placental barriers and affect the developing offspring. Phthalates are frequently prevalent as mixtures; however, most previous studies have focused on the effects of single phthalates on the ovary and female reproduction. Thus, the effects of exposure to phthalate mixtures on ovarian function and the female reproductive system remain unclear. Following a brief introduction to the ovary and its major roles, this review covers what is currently known about the effects of phthalate mixtures on the ovary, focusing primarily on their effects on folliculogenesis and steroidogenesis. Furthermore, this review focuses on the effects of phthalate mixtures on female reproductive outcomes. Finally, this review emphasizes the need for future research on the effects of environmentally relevant phthalate mixtures on the ovary and female reproduction.

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Section: Effects Of Single Phthalate and Phthalate Mixture Exposure O...mentioning

confidence: 99%

Effects of Phthalate Mixtures on Ovarian Folliculogenesis and Steroidogenesis

Fletcher

Santacruz-Márquez

Mourikes

et al. 2022

Toxics

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“…Owing to the similarity of its chemical structure with endogenous estrogen (17β-estradiol; E 2 ), the toxicity of ZEA on the female reproductive system has received widespread attention [17][18][19][20]. Relevant to the present work, some papers show that the drugs can impair PF formation [21][22][23]. Other researches have reported that PF formation can be inhibited by exposure to environmental estrogens and high concentrations of E 2 , and ZEA exposure signi cantly inhibit PF formation in embryonic stage E17.5 or postnatal 0 day (PD0) mouse ovaries [24,25].…”

Section: Introductionmentioning

confidence: 84%

Impaired primordial follicle assembly in offspring ovaries from zearalenone-exposed mothers involves reduced mitochondrial activity and altered epigenetics in oocytes

Feng

Wang

et al. 2022

Cell. Mol. Life Sci.

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Previous works have shown that zearalenone (ZEA), as an estrogenic pollutant, has adverse effects on mammalian folliculogenesis. In the present study, we found that prolonged exposure of female mice to ZEA around the end of pregnancy, caused severe impairment of primordial follicle formation in the ovaries of newborn mice and altered the expression of many genes in oocytes as revealed by scRNA-seq.These changes were associated with morphological and molecular alterations of mitochondria, increased autophagic markers in oocytes, and epigenetic changes in the ovaries of newborn mice from ZEA exposed mothers. The latter increased expression of HDAC2 deacetylases was leading to decreased levels of H3K9ac and H4K12ac. Most of these modi cations were relieved when the expression of HDAC2 in newborn ovaries was reduced by RNA interference during in vitro culture in the presence of ZEA. Such changes were also alleviated in offspring ovaries from mothers treated with both ZEA and the ubiquinone coenzyme Q10 (CoQ10), which is known to be able to restore mitochondrial activities. We concluded that impaired mitochondrial activities in oocytes caused by ZEA are at the origin of metabolic alterations that modify the expression of genes controlling autophagy and primordial follicle assembly through changes in epigenetic histones.

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“…In fact, many previous studies have confirmed that the obstruction of germ cell cyst breakdown and PF assembly are related to insufficient oocyte-specific gene expression (Wang Y. Y. et al, 2017;Wang et al, 2021;Wang J. J. et al, 2018;Liu J. C. et al, 2021). Interestingly, LH or FSH could reduce the effects of nicotine on specific gene expressions in oocytes, such as factor in the LIM homeobox 8 (Lhx8), growth differentiation factor-9 (Gdf9), spermatogenesis and oogenesis helix-loop-helix 2 (Sohlh2), and newborn ovary homeobox (Nobox; Figure 2A).…”

Section: Lh and Fsh Rescues The Impaired Oocyte-specific Gene Expressionmentioning

confidence: 99%

Protective Mechanism of Luteinizing Hormone and Follicle-Stimulating Hormone Against Nicotine-Induced Damage of Mouse Early Folliculogenesis

Liu

Zhang

Wang

et al. 2021

Front. Cell Dev. Biol.

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Previous studies have shown that nicotine could impair the germ cell cyst breakdown and the primordial follicle assembly by autophagy. In this paper, we discovered that luteinizing hormone (LH) and follicle-stimulating hormone (FSH) could counteract the damage caused by nicotine of mouse germ cell cyst breakdown. The neonatal mice were separately intraperitoneally injected with nicotine, nicotine plus LH, nicotine plus FSH, and saline (control) for 4 days. Compared with the nicotine group, the quality of oocytes and the number of follicles were remarkably increased in the nicotine plus LH group or nicotine plus FSH group. LH and FSH could alleviate nicotine-induced oocyte autophagy by different pathways. LH reduced the nicotine-induced autophagy by restoring the phosphorylation level of adenosine 5′-monophosphate-activated protein kinase α-1, while FSH by downregulating the phosphorylation level of Forkhead box class O 1. In addition, in a subsequent study of 6-week mice in different treated groups, we found that LH and FSH supplementation significantly improved normal maturation rates, fertilization rates, and embryo’s developmental potential of oocytes in oocytes exposed to nicotine. Taken together, these results suggested that LH and FSH could counteract the damage caused by nicotine and finally ensure normal germ cell cyst breakdown and early embryo development.

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Di (2-ethylhexyl) phthalate impairs primordial follicle assembly by increasing PDE3A expression in oocytes

Cited by 21 publications

References 48 publications

Effects of Phthalate Mixtures on Ovarian Folliculogenesis and Steroidogenesis

Effects of Phthalate Mixtures on Ovarian Folliculogenesis and Steroidogenesis

Impaired primordial follicle assembly in offspring ovaries from zearalenone-exposed mothers involves reduced mitochondrial activity and altered epigenetics in oocytes

Protective Mechanism of Luteinizing Hormone and Follicle-Stimulating Hormone Against Nicotine-Induced Damage of Mouse Early Folliculogenesis

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