Chemical and Toxicological Evaluations of Isolated and Synthetic Chloro Derivatives of Dibenzo-p-dioxin

Higginbotham, G R; Huang, Anita; Firestone, David; Verrett, Jacqueline; Ress, John; Campbell, A. D.

doi:10.1038/220702a0

Cited by 197 publications

(73 citation statements)

References 1 publication

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“…Cardiac abnormalities are one of the most severe teratogenicities in avian species. A mass mortality called "chick edema disease" has resulted in millions of chickens being killed with TCDD and halogenated aromatic hydrocarbon (HAH) contaminated feed (Schmittle et al 1958;Higginbotham et al 1968). …”

Section: Introductionmentioning

confidence: 99%

TCDD-induced chick cardiotoxicity is abolished by a selective cyclooxygenase-2 (COX-2) inhibitor NS398

et al. 2014

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Halogenated aromatic hydrocarbons (HAHs), including 2, 3, 7,, are known to cause severe heart defects in avian species. However, the mechanism of TCDD-induced chick cardiovascular toxicity is unclear. In this study, we investigated cyclooxygenase-2 (COX-2) as a possible mechanism of TCDD-induced cardiotoxicity. Fertile chicken eggs were injected with TCDD and a COX-2 selective inhibitor, NS398, and we investigated chick heart failure on day 10. We found that the chick heart to body weight ratio and atrial natriuretic factor (ANF) mRNA expression were increased but this increase was abolished with treatment of NS398. In addition, the morphological abnormality of an enlarged ventricle resulting from TCDD exposure was also abolished with co-treatment of TCDD and NS398. Our results suggested that TCDD-induced chick heart defects are mediated via the nongenomic pathway and that they do not require the genomic pathway.

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Section: Introductionmentioning

confidence: 99%

TCDD-induced chick cardiotoxicity is abolished by a selective cyclooxygenase-2 (COX-2) inhibitor NS398

et al. 2014

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“…When the toxicity of TCDD was first discovered, attention was directed toward its acutely lethal effects (2)(3)(4) in highly sensitive rodents such as guinea pigs (5). 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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“…The manufacture of 2,4,5-trichlorophenol, (9) found that the pyrolyzate from 2,3,4,6-tetrachlorophenol showed a GLC peak pattern resembling that displayed by some of the components of toxic fat having long retention times.…”

mentioning

confidence: 99%

“…Some commercial chlorinated phenols were found to contain chlorinated dioxins and other impurities (9,10). Industrial processes that involved heating of chlorophenols were also suspect, since under certain conditions pyrolysis of chlorophenols gave rise to dioxins.…”

mentioning

confidence: 99%

Technical pentachlorophenol: origin and analysis of base-insoluble contaminants.

Plimmer¹

1973

Environ Health Perspect

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Chemical and Toxicological Evaluations of Isolated and Synthetic Chloro Derivatives of Dibenzo-p-dioxin

Cited by 197 publications

References 1 publication

TCDD-induced chick cardiotoxicity is abolished by a selective cyclooxygenase-2 (COX-2) inhibitor NS398

TCDD-induced chick cardiotoxicity is abolished by a selective cyclooxygenase-2 (COX-2) inhibitor NS398

Linking dioxins to diabetes: epidemiology and biologic plausibility.

Technical pentachlorophenol: origin and analysis of base-insoluble contaminants.

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