ArticleToxicology and applied pharmacology2010
Flavin-containing monooxygenase-3: induction by 3-methylcholanthrene and complex regulation by xenobiotic chemicals in hepatoma cells and mouse liver.
Article in Toxicology and applied pharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 44 citations in OpenAlex.
- Flavin-containing monooxygenase (FMO): Beyond xenobiotics.BioEssays : news and reviews in molecular, cellular and developmental biology · 2024Review
- Relationship between serum trimethylamine N-oxide and exposure to dioxin-like pollutants.Environmental research · 2018Article
- Flavin-containing monooxygenases in aging and disease: Emerging roles for ancient enzymes.The Journal of biological chemistry · 2017Review
- Emerging roles of xenobiotic detoxification enzymes in metabolic diseases.Reviews on environmental health · 2017Review
- Integrated analysis of microRNA and mRNA expression profiles highlights the complex and dynamic behavior of toosendanin-induced liver injury in mice.Scientific reports · 2016Article
- Dioxin-like pollutants increase hepatic flavin containing monooxygenase (FMO3) expression to promote synthesis of the pro-atherogenic nutrient biomarker trimethylamine N-oxide from dietary precursors.The Journal of nutritional biochemistry · 2016Article
- Oxidative stress-responsive transcription factor NRF2 is not indispensable for the human hepatic Flavin-containing monooxygenase-3 (FMO3) gene expression in HepG2 cells.Toxicology in vitro : an international journal published in association with BIBRA · 2016Article
- Differential Fmo3 gene expression in various liver injury models involving hepatic oxidative stress in mice.Toxicology · 2014Article
- Tolerance to acetaminophen hepatotoxicity in the mouse model of autoprotection is associated with induction of flavin-containing monooxygenase-3 (FMO3) in hepatocytes.Toxicological sciences : an official journal of the Society of Toxicology · 2014Article
- Effects of salinity acclimation on the expression and activity of Phase I enzymes (CYP450 and FMOs) in coho salmon (Oncorhynchus kisutch).Fish physiology and biochemistry · 2014Article
- Analysis of changes in hepatic gene expression in a murine model of tolerance to acetaminophen hepatotoxicity (autoprotection).Toxicology and applied pharmacology · 2014Article
- Influence of FMO1 and 3 polymorphisms on serum olanzapine and its N-oxide metabolite in psychiatric patients.The pharmacogenomics journal · 2013Article
- Downregulation of mouse hepatic CYP3A protein by 3-methylcholanthrene does not require cytochrome P450-dependent metabolism.Drug metabolism and disposition: the biological fate of chemicals · 2013Article
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Flavin-containing monooxygenases often are thought not to be inducible but we recently demonstrated aryl hydrocarbon receptor (AHR)-dependent induction of FMO mRNAs in mouse liver by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) (Celius et al., Drug Metab Dispos 36:2499, 2008). We now evaluated FMO induction by other AHR ligands and xenobiotic chemicals in vivo and in mouse Hepa1c1c7 hepatoma cells (Hepa-1). In mouse liver, 3-methylcholanthrene (3MC) induced FMO3 mRNA 8-fold. In Hepa-1 cells, 3MC and benzo[a]pyrene (BaP) induced FMO3 mRNA >30-fold. Induction by 3MC and BaP was AHR dependent but, surprisingly, the potent AHR agonist, TCDD, did not induce FMO3 mRNA in Hepa-1 cells nor did chromatin immunoprecipitation assays detect recruitment of AHR or ARNT to Fmo3 regulatory elements after exposure to 3MC in liver or in Hepa-1 cells. However, in Hepa-1, 3MC and BaP (but not TCDD) caused recruitment of p53 protein to a p53 response element in the 5'-flanking region of the Fmo3 gene. We tested the possibility that FMO3 induction in Hepa-1 cells might be mediated by Nrf2/anti-oxidant response pathways, but agents known to activate Nrf2 or to induce oxidative stress did not affect FMO3 mRNA levels. The protein synthesis inhibitor, cycloheximide (which causes "superinduction" of CYP1A1 mRNA in TCDD-treated cells), by itself caused dramatic upregulation (>300-fold) of FMO3 mRNA in Hepa-1 suggesting that cycloheximide prevents synthesis of a labile protein that suppresses FMO3 expression. Although FMO3 mRNA is highly induced by 3MC or TCDD in mouse liver and in Hepa-1 cells, FMO protein levels and FMO catalytic function showed only modest elevation.
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