ArticleToxicology and applied pharmacology2012
Dioxin exposure reduces the steroidogenic capacity of mouse antral follicles mainly at the level of HSD17B1 without altering atresia.
Article in Toxicology and applied pharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
17 citing papers in PubMed, 49 citations in OpenAlex.
- The role of the aryl hydrocarbon receptor in ovarian development, function, xenobiotic metabolism, and disease†.Biology of reproduction · 2026Review
- Exposure to Long- and Short-Chain Per- and Polyfluoroalkyl Substances in Mice and Ovarian-Related Outcomes: AnEnvironmental health perspectives · 2025Article
- Analysis of systemic effects of dioxin on human health through template-and-anchor modeling.PLoS computational biology · 2025Article
- The role of the aryl hydrocarbon receptor in mediating the effects of mono(2-ethylhexyl) phthalate in mouse ovarian antral follicles†.Biology of reproduction · 2024Article
- Impact of dioxins on reproductive health in female mammals.Frontiers in toxicology · 2024Review
- New Gene Markers of Exosomal Regulation Are Involved in Porcine Granulosa Cell Adhesion, Migration, and Proliferation.International journal of molecular sciences · 2023Article
- Review
- Mechanisms of action of Zishen Yutai pills in treating premature ovarian failure determined by integrating UHPLC-Q-TOF-MS and network pharmacology analysis.BMC complementary medicine and therapies · 2022Article
- Endocrine Disruption of the Follicle-Stimulating Hormone Receptor Signaling During the Human Antral Follicle Growth.Frontiers in endocrinology · 2021Review
- The association between dioxins and steroid hormones in general adult males: a cross-sectional study in an e-waste region of China.Environmental science and pollution research international · 2020Article
- Endocrine disrupting chemicals: exposure, effects on human health, mechanism of action, models for testing and strategies for prevention.Reviews in endocrine & metabolic disorders · 2020Review
- Retinoic acid signaling in ovarian folliculogenesis and steroidogenesis.Reproductive toxicology (Elmsford, N.Y.) · 2019Review
- Environmental toxins and the impact of other endocrine disrupting chemicals in women's reproductive health.JBRA assisted reproduction · 2019Review
- Exposure to endocrine disruptors during adulthood: consequences for female fertility.The Journal of endocrinology · 2017Review
- EDC-2: The Endocrine Society's Second Scientific Statement on Endocrine-Disrupting Chemicals.Endocrine reviews · 2015Review
- Effects of Endocrine-Disrupting Chemicals on the Ovary.Biology of reproduction · 2015Review
- In vitro re-expression of the aryl hydrocarbon receptor (Ahr) in cultured Ahr-deficient mouse antral follicles partially restores the phenotype to that of cultured wild-type mouse follicles.Toxicology in vitro : an international journal published in association with BIBRA · 2015Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a potent ovarian toxicant. Previously, we demonstrated that in vitro TCDD (1nM) exposure decreases production/secretion of the sex steroid hormones progesterone (P4), androstenedione (A4), testosterone (T), and 17β-estradiol (E2) in mouse antral follicles. The purpose of this study was to determine the mechanism by which TCDD inhibits steroidogenesis. Specifically, we examined the effects of TCDD on the steroidogenic enzymes, atresia, and the aryl hydrocarbon receptor (AHR) protein. TCDD exposure for 48h increased levels of A4, without changing HSD3B1 protein, HSD17B1 protein, estrone (E1), T or E2 levels. Further, TCDD did not alter atresia ratings compared to vehicle at 48h. TCDD, however, did down regulate the AHR protein at 48h. TCDD exposure for 96h decreased transcript levels for Cyp11a1, Cyp17a1, Hsd17b1, and Cyp19a1, but increased Hsd3b1 transcript. TCDD exposure particularly lowered both Hsd17b1 transcript and HSD17B1 protein. However, TCDD exposure did not affect levels of E1 in the media nor atresia ratings at 96h. TCDD, however, decreased levels of the proapoptotic factor Bax. Collectively, these data suggest that TCDD exposure causes a major block in the steroidogenic enzyme conversion of A4 to T and E1 to E2 and that it regulates apoptotic pathways, favoring survival over death in antral follicles. Finally, the down-regulation of the AHR protein in TCDD exposed follicles persisted at 96h, indicating that the activation and proteasomal degradation of this receptor likely plays a central role in the impaired steroidogenic capacity and altered apoptotic pathway of exposed antral follicles.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.