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Di (2-ethylhexyl) Phthalate decrease pregnancy rate via disrupting the microbe-gut-hypothalamic-pituitary-ovarian axis in mice
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Researchers showed that DEHP, a common plasticizer, reduces pregnancy rates in mice by disrupting the gut microbiome and dysregulating the hypothalamic-pituitary-ovarian axis, with altered microbial communities elevating prostaglandin E2 and GnRH levels through increased NRG1/ErbB2 signaling in hypothalamic astrocytes.
Di (2-ethylhexyl) Phthalate (DEHP), a widely used plasticizer and endocrine disruptor, poses risks to human health, particularly reproductive function. Using a mouse model, we investigated how DEHP exposure impacts the hypothalamic-pituitary-ovarian (HPO) axis through gut microbiome disruption. DEHP decreased pregnancy rates by impairing ovarian function, activating hypothalamic astrocytes, and increasing neuregulin 1 (NRG1) expression. NRG1 binding to astrocyte ErbB2 receptors elevated prostaglandin E2 (PGE2) and gonadotropin-releasing hormone (GnRH), disrupting HPO axis homeostasis. Additionally, DEHP altered gut microbiota, destabilized microbial networks, and impacted β-glucuronidase-related taxa, leading to hormone fluctuations and reduced fertility. This study highlights gut microbiome perturbations as a novel mechanism linking DEHP exposure to reproductive dysfunction. Our study provides novel insights concerning perturbations of the gut microbiome and HPO axis and their functions as a potential new mechanism by which DEHP exposes interferes with the reproductive function-related human health.
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DEHP chronic exposure disturbs the gut microbial community and metabolic homeostasis: Gender-based differences in zebrafish
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Chronic exposure of zebrafish to DEHP — a phthalate plasticizer found in many plastic products — from embryo to adulthood disrupted gut microbial communities and metabolic balance, with effects that differed between males and females. This suggests that phthalate exposure from plastic products may alter gut health and metabolism in ways that could be relevant to human health.
Gut microbiota participates in polystyrene microplastics-induced defective implantation through impairing uterine receptivity
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Researchers found that oral exposure to polystyrene microplastics in mice impaired the ability of embryos to implant in the uterus by disrupting uterine receptivity. The study revealed that microplastics altered gut bacteria composition, which in turn affected hormone signaling and gene expression in the uterus. These findings suggest a gut-reproductive axis through which microplastic exposure could potentially affect fertility.
Associations between pre- and post-natal exposure to phthalate and DINCH metabolites and gut microbiota in one-year old children
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This study of 356 infants in the SEPAGES cohort found that urinary concentrations of several phthalate metabolites at 12 months of age were associated with higher gut microbiota diversity, with DEHP exposure additionally linked to elevated Coprococcus and Firmicutes, suggesting early-life phthalate exposure may alter the developing infant gut microbiome.
Prepregnancy Exposure to High Doses of Nanoplastics Triggers Persistent Vaginal Microbiome Dysbiosis to Induce Adverse Pregnant Outcomes
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In mice, exposure to high doses of nanoplastics before pregnancy disrupted the vaginal microbiome, causing lasting inflammation and nutrient depletion that led to miscarriage and poor embryo growth, even after the plastic particles were gone. Treatments like nutrient supplements or anti-inflammatory drugs reversed the damage, suggesting nanoplastic pollution could threaten fertility and pregnancy health, though more research is needed to confirm this in humans.
Current insights into the impact of plastic-derived pollutants (phthalates), microplastics, and nanoplastics on hypothalamic phenotype and molecular pathways: A scoping review
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This scoping review integrates evidence on how phthalates, microplastics, and nanoplastics alter hypothalamic function and neuroendocrine pathways, finding that plastic-derived pollutants disrupt metabolic regulation through hypothalamic alterations with potential systemic consequences for energy balance and reproductive function.
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