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      Daily exposure to Di(2-ethylhexyl) phthalate alters estrous cyclicity and accelerates primordial follicle recruitment potentially via dysregulation of the phosphatidylinositol 3-kinase signaling pathway in adult mice.

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          Abstract

          Humans are exposed daily to di(2-ethylhexyl) phthalate (DEHP), a plasticizer found in many consumer, medical, and building products containing polyvinyl chloride. Large doses of DEHP disrupt normal ovarian function; however, the effects of DEHP at environmentally relevant levels, the effects of DEHP on folliculogenesis, and the mechanisms by which DEHP disrupts ovarian function are unclear. The present study tested the hypothesis that relatively low levels of DEHP disrupt estrous cyclicity as well as accelerate primordial follicle recruitment by dysregulating phosphatidylinositol 3-kinase (PI3K) signaling. Adult CD-1 mice were orally dosed with DEHP (20 μg/kg/day-750 mg/kg/day) daily for 10 and 30 days. Following dosing, the effects on estrous cyclicity were examined, and follicle numbers were histologically quantified. Further, the ovarian mRNA and protein levels of PI3K signaling factors that are associated with early folliculogenesis were quantified. The data indicate that 10- and 30-day exposure to DEHP prolonged the duration of estrus and accelerated primordial follicle recruitment. Specifically, DEHP exposure decreased the percentage of primordial follicles and increased the percentage of primary follicles counted following 10-day exposure and increased the percentage of primary follicles counted following 30-day exposure. DEHP exposure, at doses that accelerate folliculogenesis, increased the levels of 3-phosphoinositide-dependent protein kinase-1, mammalian target of rapamycin complex 1, and protein kinase B and decreased the levels of phosphatase and tensin homolog, potentially driving PI3K signaling. Collectively, relatively low levels of DEHP disrupt estrous cyclicity and accelerate primordial follicle recruitment potentially via a mechanism involving dysregulation of PI3K signaling.

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          Author and article information

          Journal
          Biol Reprod
          Biology of reproduction
          Society for the Study of Reproduction
          1529-7268
          0006-3363
          Jun 2014
          : 90
          : 6
          Affiliations
          [1 ] Department of Comparative Biosciences, University of Illinois at Urbana-Champaign, Urbana, Illinois.
          [2 ] Department of Comparative Biosciences, University of Illinois at Urbana-Champaign, Urbana, Illinois jflaws@illinois.edu.
          Article
          biolreprod.114.119032
          10.1095/biolreprod.114.119032
          4435463
          24804967
          0f4c34b9-e110-4b96-a0b2-b828a8f1ad94
          © 2014 by the Society for the Study of Reproduction, Inc.
          History

          di(2-ethylhexyl) phthalate,endocrine disruptors,environmental contaminants and toxicants,follicular development,folliculogenesis,ovary,phosphatidylinositol 3-kinase signaling pathway,toxicology

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