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Classifying polycyclic aromatic hydrocarbons by carcinogenic potency using in vitro biosignatures

ABSTRACT: In this study, we compare genomic signature safter treatment ofprimary human bronchial epithelial cells (HBEC) cultured in 3D with polycyclic aromatic hydrocarbons (PAHs) and identify genesets predictive of cancer risk.

ORGANISM(S): Homo sapiens

PROVIDER: GSE156147 | GEO | 2020/10/28

REPOSITORIES: GEO

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Classifying polycyclic aromatic hydrocarbons by carcinogenic potency using in vitro biosignatures

Project description:Classifying polycyclic aromatic hydrocarbons by carcinogenic potency using in vitro biosignatures

| PRJNA656840 | ENA

Classifying polycyclic aromatic hydrocarbons by carcinogenic potency using in vitro biosignatures.

Project description:One of the most difficult challenges for risk assessment is evaluation of chemicals that predominately co-occur in mixtures like polycyclic aromatic hydrocarbons (PAHs). We previously developed a classification model in which systems biology data collected from mice short-term after chemical exposure accurately predict tumor outcome. The present study demonstrates translation of this approach into a human in vitro model in which chemical-specific bioactivity profiles from 3D human bronchial epithelial cells (HBEC) classify PAHs by carcinogenic potency. Gene expression profiles were analyzed from HBEC exposed to carcinogenic and non-carcinogenic PAHs and classification accuracies were identified for individual pathway-based gene sets. Posterior probabilities of best performing gene sets were combined via Bayesian integration resulting in a classifier with four gene sets, including aryl hydrocarbon receptor signaling, regulation of epithelial mesenchymal transition, regulation of angiogenesis, and cell cycle G2-M. In addition, transcriptional benchmark dose modeling of benzo[a]pyrene (BAP) showed that the most sensitive gene sets to BAP regulation were largely dissimilar from those that best classified PAH carcinogenicity challenging current assumptions that BAP carcinogenicity (and subsequent mode of action) is reflective of overall PAH carcinogenicity. These results illustrate utility of using systems toxicology approaches to analyze global gene expression towards carcinogenic hazard assessment.

| S-EPMC7572825 | biostudies-literature

HepG2 treated with Polycyclic Aromatic Hydrocarbons (PAHs)

2012-04-18 | GSE37326 | GEO

HepG2 treated with Polycyclic Aromatic Hydrocarbons (PAHs)

Project description:Assessing the potential carcinogenicity of human toxins represents an ongoing challenge. Chronic rodent bioassays predict human cancer risk with limited reliability, and are expensive and time-consuming. To identify alternative prediction methods, we evaluated a transcriptomics-based human in vitro model to classify carcinogens by their modes of action. The aim of this study was to determine the transcriptomic response and identify specific molecular signatures of polycyclic aromatic hydrocarbons (PAHs), which can be used as predictors of carcinogenicity of environmental toxins in human in vitro systems. We found that characteristic molecular signatures facilitate identification and prediction of carcinogens. To evaluate the change in gene expression levels, human hepatocellular carcinoma (HepG2) cells were exposed to nine different PAHs (benzo[a]pyrene, dibenzo[a,h]anthracene, 3-methylcholanthrene, naphthalene, chrysene, phenanthrene, benzo[a]anthracene, benzo[k]fluoranthene, and indeno[1,2,3-c,d]pyrene) for 48 h. Gene expression analysis was conducted using a 44K whole human genome microarray (Agilent Technologies, USA).

2012-04-17 | E-GEOD-37326 | biostudies-arrayexpress

Effects of polycyclic aromatic hydrocarbons on osteoclasts and osteoblasts in the scales of zebrafish

Project description:It has been reported that polycyclic aromatic hydrocarbons (PAHs) act on calcified tissue and suppress osteoblastic activity in the scales of teleost fish. In the present study, the differentially-expressed genes in the zebrafish scales treated with benzo[c]phenanthrene (BcP), a kind of PAH, or its metabolite 3-hydroxybenzo[c]phenanthrene (3-OHBcP) were investigated using GeneChip® oligonucleotide microarrays.

2020-11-12 | GSE161253 | GEO

Induction of active hepatic cytochrome P450 enzymes in mice exposed to benzo[a]pyrene or environmental mixtures of polycyclic aromatic hydrocarbons

Project description:Cytochrome P450 enzymes play an important role in bioactivating or detoxifying polycyclic aromatic hydrocarbons (PAHs). We exposed mice to doses of benzo[a]pyrene (BaP) or a mixture of PAHs to characterize dose- and time-response relationships of specific cytochrome P450s. Mice exposed to the highest PAH exposures exhibited 1.7-5-fold higher intrinsic clearance rates for BaP, compared to controls, and higher Vmax values, indicating higher amounts of enzymes capable of metabolizing BaP. This study demonstrates that PAHs induce enzymes in dose- and time-dependent patterns in animal models at exposure levels researchers use to characterize hazards and at relevant human exposure levels to PAH mixtures found at Superfund sites. Accounting for these potential changes in enzyme profiles, relative rates of PAH bioactivation and detoxification, and resulting risk will help reduce uncertainty and improve risk assessments for PAHs at contaminated sites.

2022-10-13 | PXD019472 | Pride

Transcription profiling of zebra fish liver after water-borne exposure to polycyclic aromatic hydrocarbons and alkylphenols

Project description:Effect of 5.4 ppm polycyclic aromatic hydrocarbons (PAHs) and 18.2 ppm alkylphenols (APs) on gene expression in adult Zebrafish (Danio rerio) liver after 1 and 7 weeks of water-borne exposure.

2008-12-11 | E-MEXP-1685 | biostudies-arrayexpress

Combined Developmental Effects of Environmental Stressors and Polycyclic Aromatic Hydrocarbons on Fundulus grandis Larvae

Project description:Oil spills have polluted the marine environment for decades and continue to be a major source of polycyclic aromatic hydrocarbons (PAHs) to marine ecosystems around the globe. Although the toxicity of PAHs to fish has been well studied, the combined effects of extreme abiotic factors and oil are poorly understood. Gulf of Mexico killifish Fundulus grandis larvae (< 24 hours post hatch) were exposed to varying environmental conditions (dissolved oxygen 2, 6 ppm; temperature 20, 25, 30°C; and salinity 3, 10, 30 ppt) combined with varying concentrations of high energy water accommodated fractions (HEWAF) (total PAHs 0 – ~ 125 ppb) for a total of 48 h. Larvae survival and development were negatively affected by PAHs, starting with the lowest concentration tested (~15 ppb). High temperature + hypoxia + PAHs resulted in the lowest survival with salinity having little impact on any of the endpoints tested. Expression of the hepatic detoxifying gene cyp1a was highly induced in PAH-exposed larvae, but only under normoxic conditions. A lack of cyp1a induction under hypoxia and PAH exposure could explain the enhanced toxicity observed. This work highlights the need for more studies examining the combined impact of suboptimal water quality parameters in the presence of pollution in fish early life-stages.

2019-04-18 | GSE129998 | GEO

Polycyclic aromatic hydrocarbons degraders

Project description:Polycyclic aromatic hydrocarbons degraders Raw sequence reads

| PRJNA590550 | ENA

Sub-chronic pulmonary transcriptional response to a mixture of 8 polycyclic aromatic hydrocarbons in adult male MutaTMMouse.

Project description:Polycyclic aromatic hydrocarbons (PAHs) are a class of hundreds of structurally similar chemicals ubiquitously present in our environment. They are created during the incomplete combustion of organic materials, such as oil, wood, tobacco, and charbroiled meat. As such, human exposure to mixtures of PAHs can occur through consumption of PAH-containing foods and water, inhalation of polluted air, or dermal contact. Several PAHs have been classified as carcinogenic to humans or probably carcinogenic to humans by the International Agency for Research on Cancer. The mice in this study were exposed to a mixture of 8 PAHs, benzo(a)pyrene, benz(a)anthracene, benzo(b)fluoranthene, benzo(ghi)perylene, benzo(k)fluoranthene, chrysene, dibenz(ah)anthracene, and indeno(123,cd)pyrene. In the present study, we sought to determine the dose-dependent changes in gene expression upon oral exposure to this PAH mixture in the lung tissue. Adult male MutaTMMouse were exposed to three doses of the mixture of 8 PAHs or vehicle control (olive oil) for 28 days and sacrificed three days after the final exposure.

2017-01-01 | GSE87689 | GEO

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