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Presence and functional activity of the aryl hydrocarbon receptor in isolated murine cerebral vascular endothelial cells and astrocytes.

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Numerous functions regulated by the central nervous system (CNS) are targeted by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD); however, the cell specific targets and mechanisms of toxicity are unknown. Outside of the brain, the peripheral vascular endothelium has been identified as a significant

Exacerbated Immune Complex-Mediated Vascular Injury in Mice with Heterozygous Deficiency of Aryl Hydrocarbon Receptor through Upregulation of Fcγ Receptor III Expression on Macrophages.

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Aryl hydrocarbon receptor (AhR), which was discovered as a receptor for environmental concomitants, plays an important role widely in the immune system. In this study, we assessed AhR involvement in immune-complex-mediated vascular injury by examining the reverse-passive Arthus reaction in AhR

The role of CYP1A inhibition in the embryotoxic interactions between hypoxia and polycyclic aromatic hydrocarbons (PAHs) and PAH mixtures in zebrafish (Danio rerio).

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Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous environmental pollutants with elevated concentrations in waters that may also experience hypoxia. Previous research has shown interactions between hypoxia and some PAHs (fluoranthene, α-naphthoflavone) but no interaction with others

Assessing Aromatic-Hydrocarbon Toxicity to Fish Early Life Stages Using Passive-Dosing Methods and Target-Lipid and Chemical-Activity Models.

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Aromatic hydrocarbons (AH) are known to impair fish early life stages (ELS). However, poorly defined exposures often confound ELS-test interpretation. Passive dosing (PD) overcomes these challenges by delivering consistent, controlled exposures. The objectives of this study were to apply PD to

Expression of the aryl hydrocarbon receptor (AhR) and AhR nuclear translocator during chick cardiogenesis is consistent with 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced heart defects.

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We examined cardiotoxicity induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in the chick embryo and the cardiac expression of transcription factors, the aryl hydrocarbon receptor (AhR) which binds TCDD, and its dimer partner, the AhR nuclear translocator (Arnt). Chicken eggs were injected with

Comparative in vivo toxicity of topical JP-8 jet fuel and its individual hydrocarbon components: identification of tridecane and tetradecane as key constituents responsible for dermal irritation.

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Despite widespread exposure to military jet fuels, there remains a knowledge gap concerning the actual toxic entities responsible for irritation observed after topical fuel exposure. The present studies with individual hydrocarbon (HC) constituents of JP-8 jet fuel shed light on this issue. To mimic

Aryl hydrocarbon receptor 2 mediates 2,3,7,8-tetrachlorodibenzo-p-dioxin developmental toxicity in zebrafish.

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In order to use the zebrafish as a model vertebrate to investigate the developmental toxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), it is essential to know whether one or both forms of the zebrafish aryl hydrocarbon receptor (AHR), zfAHR1 or zfAHR2, mediate toxicity. To determine the role

Multi-bioassay approach for assessing the potency of complex mixtures of polycyclic aromatic hydrocarbons.

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The chick embryotoxicity screening test (CHEST) and the Salmonella/microsome bioassay were used to evaluate embryotoxic and mutagenic endpoints from crude coal tar (CT) and its fractionated polycyclic aromatic hydrocarbon (PAH) mixtures (designated as A, B, C, D and E). In the CHEST assay, CT and

Microarray analysis of polychlorinated biphenyl mixture-induced changes in gene expression among Atlantic tomcod populations displaying differential sensitivity to halogenated aromatic hydrocarbons.

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Several populations of fishes inhabiting contaminated Atlantic Coast estuaries exhibit resistance to early life-stage (ELS) toxicities induced by halogenated aromatic hydrocarbons such as coplanar polychlorinated biphenyls (PCBs). These toxicities include mortality, circulatory failure, edema, and

TCDD induced pericardial edema and relative COX-2 expression in medaka (Oryzias Latipes) embryos.

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Exposure to dioxin and other aryl hydrocarbon receptor (AhR) ligands results in multiple, specific developmental cardiovascular phenotypes including pericardial edema and circulatory failure in small aquarium fish models. Although phenotypes are well described, mechanistic underpinnings for such

Alkane-induced edema formation and cutaneous barrier dysfunction.

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Certain mineral oils and hydrocarbons require repeated topical application to cause irritation. A structure activity relationship of pure n-alkanes was undertaken in a mouse ear edema model to investigate the mechanism of cumulative irritancy. Alkanes were applied twice daily over a 4-day period.

Evaluation of fish early life-stage toxicity models of chronic embryonic exposures to complex polycyclic aromatic hydrocarbon mixtures.

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Polycyclic aromatic hydrocarbons (PAHs) can cause a variety of effects in early life-stages of fish that have been chronically exposed as embryos, including mortality, deformities, and edemas. Mechanistic models of the chronic toxicity of complex mixtures of PAHs in fish have not been reported, with

Pulmonary injury after intravenous hydrocarbon injection.

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This report describes the case of a young man in whom an intravenous injection of a hydrocarbon led to reversible pulmonary edema. An 18-year-old male presented with chest pain, a cough and progressive dyspnea at a multidisciplinary paediatric intensive care unit in a tertiary care university

Aryl hydrocarbon receptor-independent toxicity of weathered crude oil during fish development.

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Polycyclic aromatic hydrocarbons (PAHs), derived largely from fossil fuels and their combustion, are pervasive contaminants in rivers, lakes, and nearshore marine habitats. Studies after the Exxon Valdez oil spill demonstrated that fish embryos exposed to low levels of PAHs in weathered crude oil

Cardiac toxicity of 5-ring polycyclic aromatic hydrocarbons is differentially dependent on the aryl hydrocarbon receptor 2 isoform during zebrafish development.

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Petroleum-derived compounds, including polycyclic aromatic hydrocarbons (PAHs), commonly occur as complex mixtures in the environment. Recent studies using the zebrafish experimental model have shown that PAHs are toxic to the embryonic cardiovascular system, and that the severity and nature of this

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