Promotion of endometriosis in mice by polychlorinated dibenzo-p-dioxins, dibenzofurans, and biphenyls.

Johnson KL, Kenneth L. Johnson, K L Johnson, A CUMMINGS, A M Cummings, Cummings AM, Linda S. Birnbaum, L S Birnbaum
Environmental health perspectives · 1997 · vol. 105(7) , pp. 750–755 · doi:10.1289/ehp.97105750 · PMID:9294722 · PMC1470109 · W2018969253
article OA: gold CC0 ⤵ 31 in-corpus citations
📄 Open PDF View on OpenAlex View on PubMed View at publisher
⚙ AI-generated summary by claude@2026-06, 2026-06-12 ⓘ

2,3,7,8-TCDD and 4-PeCDF significantly enhanced endometriotic lesion growth in mice, suggesting an Ah receptor-mediated mechanism, while PCBs 126, 153, and 1,3,6,8-TCDD had no significant effect or were confounded by ovarian toxicity.

One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works

Abstract

Previous studies showed exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD) enhances the development of endometriotic lesions. In this study we examined the effects of other polyhalogenated aromatic hydrocarbons on endometriotic proliferation. B6C3F1 female mice were treated via oral gavage a total of five times, with 3 weeks between each dosing, with 0, 1, 3, or 10 micrograms 2,3,7,8,-TCDD/kg body weight (bw); 3 or 30 mg 2,2',4,4',5,5'-hexachlorobiphenyl (PCB 153)/kg bw; 100, 300, or 1000 micrograms 3,3',4,4',5-pentachlorobiphenyl (PCB 126)/kg bw; 10, 30, or 100 micrograms 2,3,4,7,8-pentachlorodibenzofuran (4-PeCDF)/kg bw; or 2 or 20 mg 1,3,6,8-TCDD/kg at 10 ml/kg bw. Endometriosis was surgically induced during the week of the second dosing. Three weeks following the final dose, the mice were euthanized and endometriotic lesions, whole body, liver, ovaries, uterine horn, and thymus were weighted, and lesion diameters were measured. Lesions, uterine horns, and ovaries were fixed for histopathology and livers were processed for measurement of ethoxyresorufin O-deethylase (EROD) activity. Both 2,3,7,8-TCDD (1 and 3 micrograms/kg bw) and 4-PeCDF (100 micrograms/kg bw) significantly enhanced the growth of endometrial lesions. No statistically significant increase in endometriotic lesion size was detected in animals treated with either PCB 126 or with the highest dose of 2,3,7,8-TCDD, possibly due to the effects of histologically observed ovarian toxicity. The nondioxin-like compounds, PCB 153 and 1,3,6,8-TCDD, produced no observable effects on endometriosis. Hepatic EROD activity was significantly induced by 2,3,7,8-TCDD, 4-PeCDF, and PCB 126, but not by PCB 153 or 1,3,6,8-TCDD. The results of this study provide preliminary support for the hypothesis that halogenated aromatic hydrocarbon-promoted endometriosis may be Ah receptor mediated.

My notes (saved in your browser only)

Condition tags

endometriosis

MeSH descriptors

Benzofurans Endometriosis Hydrocarbons, Halogenated Polychlorinated Biphenyls Polychlorinated Dibenzodioxins Animals Benzofurans Benzofurans Cytochrome P-450 CYP1A1 Cytochrome P-450 CYP1A1 Dose-Response Relationship, Drug Endometriosis Endometriosis Female Hydrocarbons, Halogenated Hydrocarbons, Halogenated Liver Liver Mice Ovary

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

References (36)

Cited by (32)

Source provenance

europepmc
last seen: 2026-07-29T06:27:48.050232+00:00
openalex
last seen: 2026-06-10T17:14:06.276822+00:00
pubmed
last seen: 2026-05-13T22:10:46.468712+00:00
License: CC0 · commercial use OK