Toxicology of Dioxins and Related Chemicals

DeVito, Michael J.; Birnbaum, Linda S.

doi:10.1007/978-1-4899-1462-0_5

Cited by 72 publications

(56 citation statements)

References 79 publications

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“…It was relevant to the hypothesis of an association of the noted cancer occurrence pattern with TCDD exposure the fact that the largest increases for hepatobiliary cancer and hematologic neoplasms, were estimated among people residing for the longest period in the contaminated area. Notwithstanding some study limitations (lack of individual exposure markers, short latency and small population size for certain cancer types), results of previous experimental and epidemiological studies 42,51) , along with mechanistic knowledge on dioxin toxicity 52) , corroborate the hypotheses that the observed excesses from neoplastic causes, although based on a small number of deaths, might be associated with dioxin exposure.…”

Section: Morbiditysupporting

confidence: 57%

Short- and Long-Term Morbidity and Mortality in the Population Exposed to Dioxin after the "Seveso Accident".

et al. 2003

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The early effects of 2,3,7,8-tetrachlorodibenzo-para-dioxin (TCDD) exposure in the population involved in the Seveso, Italy, incident in 1976, have been examined in numerous studies. Chloracne was the only effect linked with sufficient certainty to dioxin exposure. The possible longterm consequences were investigated with mortality and cancer incidence studies. Mortality and morbidity findings during the 20-year period following the accident showed increased risk from lymphoemopoietic neoplasm, digestive system cancer (rectum in males, and biliary tract among females, in particular) and respiratory system cancer (lung, among males). In the incidence analyses, also thyroid gland and pleura cancer appeared suggestively increased. Soft tissue sarcomas showed an increase in the largest, yet least exposed, exposure sub-cohort. Several hypotheses associating non-cancer effects with dioxin exposure were corroborated by findings in the Seveso population: this was the case with cardiovascular effects (possibly linked to both chemical exposure and stressful disaster experience), endocrine effects (diabetes among females) and reproductive effects: exposure of men to TCDD was linked to a lowered male/female sex ratio in their offspring. The results of many Seveso studies point to possible gender effects, in accordance with animal models. Notwithstanding the acknowledged study limitations (lack of individual exposure markers, short latency, and small population size for certain cancer types), results of previous experimental and epidemiological studies, along with mechanistic knowledge on dioxin toxicity, support the hypotheses that the observed excesses might be associated with dioxin exposure. The mortality and cancer incidence follow-up of the Seveso cohort are continuing.

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Section: Morbiditysupporting

confidence: 57%

Short- and Long-Term Morbidity and Mortality in the Population Exposed to Dioxin after the "Seveso Accident".

et al. 2003

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“…Since many hormones play important roles at each stage, exogenous environmental chemicals that mimic, inhibit or modulate endogenous chemical messengers can influence development. Dioxin alters cell growth and differentiation by affecting homeostasis and hormone balance through modulation of enzyme induction, growth factors, hormones and their receptors 6) . TCDD acts in an estrogenic or anti-estrogenic manner depending on the tissues and developmental stage 7,8) .…”

Section: The Mechanism Of Dioxin's Action and The Developmental Processmentioning

confidence: 99%

The Effects of Dioxin on Reproduction and Development.

Yonemoto

2000

INDUSTRIAL HEALTH

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The developmental effects of dioxin are important because of the high sensitivity of mammals as well as the irreversibility and longevity of the effects. In animal experiments, exposure to dioxin during pregnancy and lactation induce various functional effects on offspring at very low doses. In humans, even if there is no exposure to dioxin after birth, there might be effects on thyroid function in infants exposed to dioxin from breast milk. In this report, low-dose developmental effects of dioxins on offspring in animal experiments and human studies were reviewed. In terms of risk assessment, methods to describe dosimetry, models to describe dose-response and approaches to express health risk are discussed.

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“…1) Dioxins bind to the cytosolic aryl hydrocarbon receptor (AhR), commonly called the dioxin receptor, resulting in its transformation. [2][3][4] The transformed AhR works as a transcriptional factor after entering the nucleus, forming a heterodimer with the AhR nuclear translocator (Arnt), and binding to a DNA sequence called dioxin responsive element (DRE). [5][6][7] These sequential actions lead to the expression of various proteins, including drug-metabolizing enzymes such as cytochrome P450 1A1 (CYP1A1), glutathione S-transferase (GST), and NAD(P)H:quinone-oxidoreductase (NQO1).…”

mentioning

confidence: 99%

Black Tea Theaflavins Suppress Dioxin-Induced Transformation of the Aryl Hydrocarbon Receptor

Fukuda

Sakane

Yabushita

et al. 2005

Bioscience, Biotechnology, and Biochemistry

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Dioxins cause various adverse effects through transformation of aryl hydrocarbon receptor (AhR). In this study, we investigated whether black tea extract and its components, theaflavins, suppress AhR transformation in vitro. First, we confirmed that black tea extract strongly suppressed AhR transformation compared to green and oolong tea, although the catechin contents did not change significantly among the extracts. Then we isolated four theaflavins as active compounds from black tea leaves. They suppressed 1 nM 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced AhR transformation in a dose-dependent manner. The IC 50 values of theaflavin, theaflavin-3-gallate, theaflavin-3 0 -gallate, and theaflavin-3,3 0 -digallate (Tfdg) were 4.5, 2.3, 2.2, and 0.7 M, respectively. The suppressive effect of Tfdg was observed not only by pre-treatment but also by posttreatment. This suggests that theaflavins inhibit the binding of TCDD to the AhR and also the binding of the transformed AhR to the specific DNA-binding site as putative mechanisms.

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Toxicology of Dioxins and Related Chemicals

Cited by 72 publications

References 79 publications

Short- and Long-Term Morbidity and Mortality in the Population Exposed to Dioxin after the "Seveso Accident".

Short- and Long-Term Morbidity and Mortality in the Population Exposed to Dioxin after the "Seveso Accident".

The Effects of Dioxin on Reproduction and Development.

Black Tea Theaflavins Suppress Dioxin-Induced Transformation of the Aryl Hydrocarbon Receptor

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