ArticleArchives of toxicology2025
Evaluating CYP enzyme induction by cigarette smoking: a new in vitro approach using primary human hepatocytes.
Article in Archives of toxicology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- CYP1A1 as a conserved metabolic circuit linking environmental sensing to immune regulation.Archives of toxicology · 2026Review
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cigarette smoke contains compounds that significantly affect drug interactions in clinical settings, primarily through the induction of cytochrome P450 (CYP) enzymes. Given the complexity of cigarette smoke, use of cigarette smoke extract (CSE) in in vitro systems is essential for mimicking in vivo effects and analyzing CYP enzyme induction. Regulatory authorities recommend testing drug-drug interactions; however, there is currently no in vitro model to study smoke-drug interactions. This study developed a model using primary human hepatocytes (PHH) to analyze CYP enzyme induction by CSE inspired by the ICH M12 (2024) guideline. The robustness of the model was evaluated by analyzing the effects of CSE derived from three lots of research cigarettes on three PHH donors. The parameters of CSE production were optimized for a 2.5-min cigarette burning and a cell culture medium as CSE solvent. A reliable, concentration-dependent induction of CYP1A1 and CYP1A2 by CSE across different donors and cigarettes was verified based on an enzyme activity (LC-MS/MS) and mRNA expression levels (qRT-PCR). The strongest induction was observed for CYP1A1 mRNA with at least 15-fold, and CYP1A1 enzyme activity with at least 57-fold induction, across all donors. Protein levels of induced CYP1A1 in PHH were comparable to those of non-induced CYP1A2. Therefore, the data suggest a notable role of induced CYP1A1 in liver metabolism. Additionally, CSE induced the mRNA expression levels of CYP2B6, CYP2C8, and CYP3A4. This model has the potential to provide in vitro smoke-drug interaction results prior to clinical trials and can therefore assist in clinical study planning.
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Registered trials
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