Exposure to di(2-ethylhexyl) phthalate and diisononyl phthalate alters the aryl hydrocarbon receptor signaling pathway in the ovary throughout reproductive aging in mice

Clicks: 14
ID: 329896
2026
Free PDF
Article Quality & Performance Metrics
Overall Quality
Not rated
Combines reader engagement with the AI quality analysis. This article has not been analysed, so there is no overall score — reader engagement is measured and shown alongside.
AI Quality Assessment
Not analyzed
Readership in this journal
Emerging

Ranked #95 of 143 articles by views in toxicological sciences : an official journal of the society of toxicology

Most read Least read

Bar heights use a square-root scale. Only the 120 most-read articles are drawn; the journal has 143 in total.

Mint this article as an NFT
Not yet minted

Create a permanent, verifiable on-chain record of this article on the Scimatic Network. The NFT is held in your Journament account, and you can withdraw it to your own wallet at any time.

5 SUSD one-off · no wallet required
Sign in to mint
Abstract
Di(2-ethylhexyl) phthalate (DEHP) and diisononyl phthalate (DiNP) are plasticizers used in many consumer products. Both phthalates alter estrous cyclicity, fertility indices, and folliculogenesis throughout the reproductive lifespan. Our companion paper showed that exposure to a phthalate mixture containing DEHP and DiNP altered the aryl hydrocarbon receptor (AHR) signaling pathway in the ovary. However, limited information was available on how DEHP and DiNP individually affect the AHR signaling pathway in the ovary throughout reproductive aging. Thus, we hypothesized that DEHP and DiNP individually affect the gene and protein expression and localization associated with the AHR pathway throughout the reproductive lifespan. We treated adult female CD-1 mice with corn oil control or doses (0.15 ppm, 1.5 ppm, or 1500 ppm) of DEHP and DiNP in the diet for 1-12 months. Sera were used to measure circulating estradiol (E2) concentrations. The AHR pathway was assessed using quantitative PCR (qPCR) for gene expression, RNAscopeTM in situ hybridization for transcript localization, and immunohistochemistry for protein localization. Exposure to DEHP, but not DiNP, reduced serum E2 after 1 month compared to control. DEHP exposure increased Cyp1a1 expression and CYP1B1 localization in the ovary after 6 months compared to control. DiNP also increased Arnt expression and CYP1B1 localization in the ovary after 1 month compared to control. DiNP exposure decreased Ahr and Cyp1a1 expression as well as CYP1A1 localization in the antral follicle after 12 months compared to control. Overall, DEHP and DiNP both influence the ovarian AHR pathway, but at different time points and doses.
Reference Key
openalex_W7214449646 Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Angela Elizabeth Dean, Ramsés Santacruz-Márquez, Adira M Safar, Mary J. Laws, Taylor A Seaton, Estella Miller, Justin Huff, Lydia M Hall, Jodi A Flaws
Journal toxicological sciences : an official journal of the society of toxicology
Year 2026
DOI
10.1093/toxsci/kfag131
URL
https://doi.org/10.1093/toxsci/kfag131
Keywords Keywords not found

Citations

No citations found. To add a citation, contact the admin at info@scimatic.org

Comments

No comments yet. Be the first to comment on this article.