ArticleMutation research. Genetic toxicology and environmental mutagenesis2020
Enhanced DNA adduct formation by benzo[a]pyrene in human liver cells lacking cytochrome P450 oxidoreductase.
Article in Mutation research. Genetic toxicology and environmental mutagenesis, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 14 citations in OpenAlex.
- Bread crust extract is a novel activator of aryl hydrocarbon receptor and modulator of NRF2 and NFκB in HepG2 and HCT 116 cells.Current research in food science · 2025Article
- Review
- Protective Effect of the Hydrophilic Extract ofAntioxidants (Basel, Switzerland) · 2022Article
- Effects of benzo[a]pyrene exposure on black rockfish (Sebastes schlegelii): EROD activity, CYP1A protein, and immunohistochemical and histopathological alterations.Environmental science and pollution research international · 2022Article
- Applications of Adductomics in Chemically Induced Adverse Outcomes and Major Emphasis on DNA Adductomics: A Pathbreaking Tool in Biomedical Research.International journal of molecular sciences · 2021Review
- Benzo[International journal of molecular sciences · 2021Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diet is a major source of human exposure to polycyclic aromatic hydrocarbons (PAHs), of which benzo[a]pyrene (BaP) is the most commonly studied and measured. BaP has been considered to exert its genotoxic effects after metabolic activation by cytochrome P450 (CYP) enzymes whose activity can be modulated by cytochrome P450 oxidoreductase (POR), the electron donor to CYP enzymes. Previous studies showed that BaP-DNA adduct formation was greater in the livers of Hepatic Reductase Null (HRN) mice, in which POR is deleted specifically in hepatocytes, than in wild-type (WT) mice. In the present study we used human hepatoma HepG2 cells carrying a knockout (KO) in the POR gene as a human in vitro model that can mimic the HRN mouse model. Treatment to BaP for up to 48 h caused similar cytotoxicity in POR KO and WT HepG2 cells. However, levels of BaP activation (i.e. BaP-7,8-dihydrodiol formation) were higher in POR KO HepG2 cells than in WT HepG2 cells after 48 h. This also resulted in substantially higher BaP-DNA adduct formation in POR KO HepG2 cells indicating that BaP metabolism is delayed in POR KO HepG2 cells thereby prolonging the effective exposure of cells to unmetabolized BaP. As was seen in the HRN mouse model, these results suggest that cytochrome b
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