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Related Concept Videos

Teratogenicity01:07

Teratogenicity

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The ability of a drug to produce structural deformations and functional abnormalities in the developing embryo or the fetus is called teratogenicity, and the drug producing this effect is known as a teratogen. Teratogenic effects include stillbirth, miscarriage, intrauterine growth restriction, and neurocognitive delay. A teratogen may affect the embryo at different stages of development, which is important in determining the type and extent of the damage. During blastocyst formation, the early...
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Collection of Alfalfa Root Exudates to Study the Impact of Di2-ethylhexyl Phthalate on Metabolite Production
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Di (2-ethylhexyl) Phthalate decrease pregnancy rate via disrupting the microbe-gut-hypothalamic-pituitary-ovarian

Linjie Xu1, Jun Yan2, Tingting Yin2

  • 1Department of Obstetrics, Women's Hospital of Nanjing Medical University, Nanjing Women and Children's Healthcare Hospital, Nanjing, Jiangsu, PR China. linjiexu@njmu.edu.cn.

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|June 13, 2025
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Summary
This summary is machine-generated.

Di (2-ethylhexyl) phthalate (DEHP) exposure reduces fertility by disrupting the gut microbiome and the hypothalamic-pituitary-ovarian (HPO) axis. This plasticizer impairs ovarian function and alters key hormone signaling pathways, impacting reproductive health.

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Area of Science:

  • Endocrinology
  • Microbiology
  • Toxicology

Background:

  • Di (2-ethylhexyl) phthalate (DEHP) is a common plasticizer and endocrine disruptor linked to reproductive health risks.
  • The hypothalamic-pituitary-ovarian (HPO) axis regulates reproductive function and is sensitive to environmental exposures.
  • Gut microbiome alterations are increasingly recognized as contributing factors to various health issues, including endocrine disruption.

Purpose of the Study:

  • To investigate the impact of DEHP exposure on the HPO axis via gut microbiome disruption in a mouse model.
  • To elucidate the specific molecular mechanisms by which DEHP affects reproductive function.
  • To identify novel pathways linking environmental contaminants to reproductive dysfunction.

Main Methods:

  • Exposure of mice to DEHP.
  • Assessment of reproductive parameters, including pregnancy rates and ovarian function.
  • Analysis of HPO axis components, including hypothalamic astrocyte activation and neuregulin 1 (NRG1) expression.
  • Investigation of gut microbiota composition and function, focusing on β-glucuronidase-related taxa.
  • Measurement of prostaglandin E2 (PGE2) and gonadotropin-releasing hormone (GnRH) levels.

Main Results:

  • DEHP exposure significantly decreased pregnancy rates and impaired ovarian function.
  • DEHP activated hypothalamic astrocytes and increased NRG1 expression, leading to elevated PGE2 and GnRH.
  • DEHP altered gut microbiota, destabilized microbial networks, and affected β-glucuronidase-related taxa, correlating with hormone fluctuations.
  • These changes collectively disrupted HPO axis homeostasis and reduced fertility.

Conclusions:

  • Gut microbiome perturbations represent a novel mechanism by which DEHP exposure interferes with reproductive function.
  • DEHP-induced disruption of the HPO axis involves NRG1-mediated signaling and alterations in gut microbial communities.
  • Understanding these pathways provides critical insights into the reproductive health risks associated with phthalate exposure.