The Effects of Dioxin on Reproduction and Development.

Yonemoto, Junzo

doi:10.2486/indhealth.38.259

Cited by 36 publications

(17 citation statements)

References 76 publications

(66 reference statements)

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“…Exposure to the halogenated aromatic hydrocarbon, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), elicits a number of biological and toxicological responses which include both endocrine disruptive effects and cancer (1)(2)(3). In particular, recent animal experiments have demonstrated a number of female reproductive toxicities resulting from TCDD exposure, including induction of ovarian tumors in rats, placental hypoxia in pregnant rats and inhibition of estradiol secretion from human luteinizing granulosa cells (4)(5)(6).…”

Section: Introductionmentioning

confidence: 99%

Activation of telomerase in BeWo cells by estrogen and 2,3,7,8-tetrachlorodibenzo-p-dioxin in co-operation with c-Myc

Sarkar

Shiizaki²,

Yonemoto³

et al. 2006

Int J Oncol

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Abstract. Telomerase activation, known to be stimulated by estrogen, is essential for cellular immortalization and transformation, both of which play a role in tumorigenesis. Dioxin and dioxin-like compounds have been shown to induce endometriosis and promote estrogen-dependent tumors. In this study, we show that either 2,3,7,8-tetrachlorodibenzo-pdioxin (TCDD) or a combination of TCDD and 17-ß estradiol (E2) increase telomerase activity and the expression of the human telomerase catalytic subunit (hTERT) in human choriocarcinoma (BeWo) cells. Compared with estrogen or TCDD alone, the combination treatment did not show an additive effect. Likewise, treatment with either E2 or TCDD increased DNA synthesis and the cell population in S-phase, as detected by FACS analysis. However, following treatment with the E2 and TCDD combination, the proportion of cells in S-phase was actually lower than in cells treated with TCDD alone. These results suggest that TCDD alone mimics estrogenic action in telomerase activation and cell proliferation but, in the presence of estrogen, TCDD-induced actions were partially counteracted. E2 and TCDD also induced c-Myc, which is a transcriptional activator of hTERT in BeWo, but neither of these agents induced telomerase activity in HO15.19 c-myc-null cells. In contrast, only TCDD upregulated telomerase in TGR-1 cells, which are c-Myc expressing but lacking ER expression. The findings suggest that TCDD induces telomerase activity mediated through AhR signaling and/or ER-independent c-Myc signaling. The present study provides insight into the mechanism of promoter activity of TCDD in estrogen-related tumors.

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Section: Introductionmentioning

confidence: 99%

Activation of telomerase in BeWo cells by estrogen and 2,3,7,8-tetrachlorodibenzo-p-dioxin in co-operation with c-Myc

Sarkar

Shiizaki²,

Yonemoto³

et al. 2006

Int J Oncol

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“…The realization that human beings are less susceptible to these acute effects shifted the focus to lowlevel chronic effects such as carcinogenicity (6) and reproductive toxicity (7,8), both of which can be induced in animal models at concentrations close to those to which humans are exposed (9).…”

mentioning

confidence: 99%

Linking dioxins to diabetes: epidemiology and biologic plausibility.

Remillard

Bunce

2002

Environ Health Perspect

180

115

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Recent epidemiologic studies suggest a possible association between dioxin-like compounds (DLCs) and diabetes in human populations, although experimental links between DLCs and diabetes are lacking. The public health significance of such an association is that all populations are exposed to small but measurable levels of DLCs, chronic low-dose exposure to which may hasten the onset of adult-onset diabetes in susceptible individuals. In this article, we review the epidemiologic studies and propose biologically plausible connections between dioxins and diabetes. Specifically, we suggest that aryl hydrocarbon (Ah) receptor functions may antagonize peroxisome proliferator-activated receptor (PPAR) functions, and hence that the Ah receptor may promote diabetogenesis through a mechanism of PPAR antagonism.

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“…Hexacholorobenzene, found in Great Lakes waters, may be associated with damage to the structure of the ovary (34) and pesticides have been linked with reproductive failure in animals (36) and humans (37)(38)(39).…”

Section: Diseases Of the Reproductive Organsmentioning

confidence: 99%