{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Rude CI"],"funding":["National Institute of Environmental Health Sciences","NIEHS NIH HHS","National Institutes of Health","NIH HHS"],"pagination":["50-68"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11514837"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["202(1)"],"pubmed_abstract":["Polycyclic aromatic hydrocarbons (PAHs) are a class of organic compounds frequently detected in the environment with widely varying toxicities. Many PAHs activate the aryl hydrocarbon receptor (AHR), inducing the expression of a battery of genes, including xenobiotic metabolizing enzymes like cytochrome P450s (CYPs); however, not all PAHs act via this mechanism. We screened several parent and substituted PAHs in in vitro AHR activation assays to classify their unique activity. Retene (1-methyl-7-isopropylphenanthrene) displays Ahr2-dependent teratogenicity in zebrafish, but did not activate human AHR or zebrafish Ahr2, suggesting a retene metabolite activates Ahr2 in zebrafish to induce developmental toxicity. To investigate the role of metabolism in retene toxicity, studies were performed"],"journal":["Toxicological sciences : an official journal of the Society of Toxicology"],"pubmed_title":["Aryl hydrocarbon receptor-dependent toxicity by retene requires metabolic competence."],"pmcid":["PMC11514837"],"funding_grant_id":["T32 ES007060","P42 ES016465","P30 ES030287"],"pubmed_authors":["Wilson LB","La Du J","Schultz KJ","Rude CI","Colby SM","Smith JN","Lalli PM","Tanguay RL","Waters KM"],"additional_accession":[]},"is_claimable":false,"name":"Aryl hydrocarbon receptor-dependent toxicity by retene requires metabolic competence.","description":"Polycyclic aromatic hydrocarbons (PAHs) are a class of organic compounds frequently detected in the environment with widely varying toxicities. Many PAHs activate the aryl hydrocarbon receptor (AHR), inducing the expression of a battery of genes, including xenobiotic metabolizing enzymes like cytochrome P450s (CYPs); however, not all PAHs act via this mechanism. We screened several parent and substituted PAHs in in vitro AHR activation assays to classify their unique activity. Retene (1-methyl-7-isopropylphenanthrene) displays Ahr2-dependent teratogenicity in zebrafish, but did not activate human AHR or zebrafish Ahr2, suggesting a retene metabolite activates Ahr2 in zebrafish to induce developmental toxicity. To investigate the role of metabolism in retene toxicity, studies were performed","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Nov","modification":"2026-07-07T03:17:43.374Z","creation":"2026-07-07T03:10:44.042Z"},"accession":"S-EPMC11514837","cross_references":{"pubmed":["39107868"],"doi":["10.1093/toxsci/kfae098"]}}