ArticleArchives of toxicology2016
New insights into BaP-induced toxicity: role of major metabolites in transcriptomics and contribution to hepatocarcinogenesis.
Article in Archives of toxicology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.
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Who cites it
30 citing papers in PubMed, 1 synthesis or guideline pooled it, 101 citations in OpenAlex.
- Meta-analysis identifies key genes and pathways implicated in Benzo[a]pyrene exposure response.Chemosphere · 2024Pooled it
- Transcriptomic Analysis Reveals Core Genes and Mechanisms Linking Grilled Food Toxicants (4-HNE, BaP, PhIP) to NASH-HCC Progression.Food science & nutrition · 2026Article
- Aryl hydrocarbon receptor: a multifaceted environmental sensor in liver homeostasis and disease.Frontiers in medicine · 2026Review
- Ecotoxicological impacts of benzo[a]pyrene onFrontiers in immunology · 2026Article
- Exploring the Activation of the Keap1-Nrf2-ARE Pathway by PAHs in Children's Toys.Contact dermatitis · 2025Article
- A Multicomponent Reaction-Based Platform Opens New Avenues in Aryl Hydrocarbon Receptor Modulation.ACS central science · 2025Article
- Article
- Exposure of benzo[a]pyrene induces HCC exosome-circular RNA to activate lung fibroblasts and trigger organotropic metastasis.Cancer communications (London, England) · 2024Article
- Benzo[a]pyrene-induced multigenerational changes in gene expression, behavior, and DNA methylation are primarily influenced by paternal exposure.Toxicology and applied pharmacology · 2023Article
- Benzo[Frontiers in immunology · 2023Article
- Unraveling the differential impact of PAHs and dioxin-like compounds on AKR1C3 reveals the EGFR extracellular domain as a critical determinant of the AHR response.Environment international · 2022Article
- The influencing factors of health hazards of benzo[a]pyrene in cigarette mainstream smoke: The example of one brand in Beijing.Tobacco induced diseases · 2022Article
- Concentration-response gene expression analysis in zebrafish reveals phenotypically-anchored transcriptional responses to retene.Frontiers in toxicology · 2022Article
- The effect of benzo[a]pyrene on the gut microbiota of Nile tilapia (Oreochromis niloticus).Applied microbiology and biotechnology · 2021Article
- Benzo[a]pyrene stimulates miR-650 expression to promote the pathogenesis of fatty liver disease and hepatocellular carcinoma via SOCS3/JAK/STAT3 cascades.Journal of molecular cell biology · 2021Article
- Identification of a five-immune gene model as an independent prognostic factor in hepatocellular carcinoma.BMC cancer · 2021Article
- Article
- Targeting glutathione with the triterpenoid CDDO-Im protects against benzo-a-pyrene-1,6-quinone-induced cytotoxicity in endothelial cells.Molecular and cellular biochemistry · 2020Article
- Protective Effects of Myricetin on Benzo[a]pyrene-Induced 8-Hydroxy-2'-Deoxyguanosine and BPDE-DNA Adduct.Antioxidants (Basel, Switzerland) · 2020Article
- Modulatory Effects of Silymarin on Benzo[a]pyrene-Induced Hepatotoxicity.International journal of molecular sciences · 2020Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Benzo(a)pyrene (BaP) is a ubiquitous carcinogen resulting from incomplete combustion of organic compounds and also present at high levels in cigarette smoke. A wide range of biological effects has been attributed to BaP and its genotoxic metabolite BPDE, but the contribution to BaP toxicity of intermediary metabolites generated along the detoxification path remains unknown. Here, we report for the first time how 3-OH-BaP, 9,10-diol and BPDE, three major BaP metabolites, temporally relate to BaP-induced transcriptomic alterations in HepG2 cells. Since BaP is also known to induce AhR activation, we additionally evaluated TCDD to source the expression of non-genotoxic AhR-mediated patterns. 9,10-Diol was shown to activate several transcription factor networks related to BaP metabolism (AhR), oxidative stress (Nrf2) and cell proliferation (HIF-1α, AP-1) in particular at early time points, while BPDE influenced expression of genes involved in cell energetics, DNA repair and apoptotic pathways. Also, in order to grasp the role of BaP and its metabolites in chemical hepatocarcinogenesis, we compared expression patterns from BaP(-metabolites) and TCDD to a signature set of approximately nine thousand gene expressions derived from hepatocellular carcinoma (HCC) patients. While transcriptome modulation by TCDD appeared not significantly related to HCC, BaP and BPDE were shown to deregulate metastatic markers via non-genotoxic and genotoxic mechanisms and activate inflammatory pathways (NF-κβ signaling, cytokine-cytokine receptor interaction). BaP also showed strong repression of genes involved in cholesterol and fatty acid biosynthesis. Altogether, this study provides new insights into BaP-induced toxicity and sheds new light onto its mechanism of action as a hepatocarcinogen.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.