Promotion of Endometriosis in Mice by Polychlorinated Dibenzo-p-Dioxins, Dibenzofurans, and Biphenyls

Johnson, Krista L.; Cummings, Audrey M.; Birnbaum, Linda S.

doi:10.2307/3433731

Cited by 13 publications

(18 citation statements)

References 21 publications

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“…On the other hand, B6C3F1 mice treated with 0, 1.5, or 150 ng/kg TCDD showed no adverse effects in body weights or organ/body weight ratios (Diliberto et al, 2001). In agreement with other studies in mice and rats, we noted a decreased ovarian weight (Johnson et al, 1997;Cummings et al, 1999), which is likely due to a direct influence of TCDD on the ovary (Heiden et al, 2006). Lower E2 levels were found in the TCDD-treated groups.…”

Section: Discussionsupporting

confidence: 80%

Proteomic Analysis of the Rat Ovary Following Chronic Low-Dose Exposure to 2,3,7,8-Tetrachlorodibenzo-p-Dioxin (TCDD)

Chen

et al. 2009

Journal of Toxicology and Environmental Health, Part A

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Section: Discussionsupporting

confidence: 80%

Proteomic Analysis of the Rat Ovary Following Chronic Low-Dose Exposure to 2,3,7,8-Tetrachlorodibenzo-p-Dioxin (TCDD)

Chen

et al. 2009

Journal of Toxicology and Environmental Health, Part A

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“…Although there are some dioxin-like PCBs in Aroclor 1254, most of the PCBs have no dioxin-like activity. Therefore, in agreement with the studies of Johnson et al (37), one would not expect endometriosis in this cohort. Another explanation may be that the Canadian monkeys were not held long enough for the endometriosis to become apparent.…”

Section: Review • Birnbaum and Cummingssupporting

confidence: 92%

“…Doses were selected on the basis of the relative potency of these congeners to TCDD. The study by Johnson et al (37), which predated the World Health Organization publication of relative TEF values, used enzyme data obtained in Birnbaum's laboratory to determine relative potency. TCDD, 4PeCDF, and PCB 126 all promoted the growth of the endometrial implants (Figure 2).…”

Section: Review • Birnbaum and Cummingsmentioning

confidence: 99%

Dioxins and endometriosis: a plausible hypothesis.

Birnbaum

Cummings

2002

Environ Health Perspect

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A potential connection exists between exposure to organochlorine chemicals and the increasing prevalence of endometriosis. Evidence shows that dioxin (2,3,7,8-tetrachlorodibenzo-p-dioxin) can increase the incidence and severity of the disease in monkeys and can promote the growth or survival of endometrial tissue implanted into rodents in a surgically induced model of endometriosis. The mechanism of the connection between organochlorine chemicals and endometriosis is not clear. Effects on growth factors, cytokines, and hormones (components of the immune and endocrine systems) are potential means of mediating the possible promotion of endometriosis by dioxins. Studies on epidemiology and on structure-activity relationships of organochlorine chemicals and endometriosis have been additional approaches to this problem. In this regard, toxic equivalence (TEQ) appears to be an important determinant of the effects of organochlorine chemicals on endometriosis. In this article, we review the literature related to endometriosis and dioxins and attempt to integrate the various sources of information that bolster the hypothesis connecting dioxins and endometriosis.

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“…Environmental AhR ligands have been implicated in promoting endometriosis and endometrial cancer in various species (Cummings et al 1996, Johnson et al 1997, Mann 1997, Mayani et al 1997, Rier 2002). Yet, epidemiological data from the accidental exposure to TCDD in Seveso, Italy (1976), have revealed a decrease in the incidence of endometrial carcinoma in TCDD-exposed women (Bertazzi et al 1997).…”

Section: Ahr Cross-talk With Steroid Hormone Receptorsmentioning

confidence: 99%

Molecular interactions of the aryl hydrocarbon receptor and its biological and toxicological relevance for reproduction

Pocar

Fischer²,

Klonisch³

et al. 2005

Reproduction

167

126

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The dioxin/aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor responsive to both natural and man-made environmental compounds. AhR and its nuclear partner ARNT are expressed in the female reproductive tract in a variety of species and several indications suggest that the AhR might play a pivotal role in the physiology of reproduction. Furthermore, it appears to be the mediator of most, if not all, the adverse effects on reproduction of a group of highly potent environmental pollutants collectively called aryl hydrocarbons (AHs), including the highly toxic compound 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Although a large body of recent literature has implicated AhR in multiple signal transduction pathways, the mechanisms of action resulting in a wide spectrum of effects on female reproduction are largely unknown. Here we summarize the major types of molecular cross-talks that have been identified for the AhR and linked cell signaling pathways and that are relevant for the understanding of the role of this transcription factor in female reproduction.

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Promotion of Endometriosis in Mice by Polychlorinated Dibenzo-p-Dioxins, Dibenzofurans, and Biphenyls

Cited by 13 publications

References 21 publications

Proteomic Analysis of the Rat Ovary Following Chronic Low-Dose Exposure to 2,3,7,8-Tetrachlorodibenzo-p-Dioxin (TCDD)

Proteomic Analysis of the Rat Ovary Following Chronic Low-Dose Exposure to 2,3,7,8-Tetrachlorodibenzo-p-Dioxin (TCDD)

Dioxins and endometriosis: a plausible hypothesis.

Molecular interactions of the aryl hydrocarbon receptor and its biological and toxicological relevance for reproduction

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