Cited by 103Drug-Induced Hepatotoxicity and ProtectionPharmacogenetics and Drug MetabolismDrug Transport and Resistance Mechanisms

Development of HepG2-derived cells expressing cytochrome P450s for assessing metabolism-associated drug-induced liver toxicity

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Xuan, Jiekun, Chen, Si, Ning, Baitang, Tolleson, William H., Guo, Lei·2016·Chemico-Biological Interactions

Abstract

The generation of reactive metabolites from therapeutic agents is one of the major mechanisms of drug-induced liver injury (DILI). In order to evaluate metabolism-related toxicity and improve drug efficacy and safety, we generated a battery of HepG2-derived cell lines that express 14 cytochrome P450s (CYPs) (1A1, 1A2, 1B1, 2A6, 2B6, 2C8, 2C9, 2C18, 2C19, 2D6, 2E1, 3A4, 3A5 and 3A7) individually using a lentiviral expression system. The expression/production of a specific CYP in each cell line was confirmed by an increased abundance of the CYP at both mRNA and protein levels. Moreover, the enzymatic activities of representative CYPs in the corresponding cell lines were also measured. Using our CYP-expressed HepG2 cells, the toxicity of three drugs that could induce DILI (amiodarone, chlorpromazine and primaquine) was assessed, and all of them showed altered (increased or decreased) toxicity compared to the toxicity in drug-treated wild-type HepG2 cells. CYP-mediated drug toxicity examined in our cell system is consistent with previous reports, demonstrating the potential of these cells for assessing metabolism-related drug toxicity. This cell system provides a practical in vitro approach for drug metabolism screening and for early detection of drug toxicity. It is also a surrogate enzyme source for the enzymatic characterization of a particular CYP that contributes to drug-induced liver toxicity.

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Crossref · 10.1016/j.cbi.2015.10.009

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  • HepG2 is suitable for studying general mechanisms of cytotoxicity and cellular stress response but limited for quantitative prediction of metabolism and biotransformation of many compounds.

    “Recent reviews and experimental studies directly interpret HepG2 as a model suitable for solving certain toxicological problems, in particular for studying general mechanisms of cytotoxicity and cellular stress response (e.g., activation of transcription factors activator protein-1 (AP1), p53, nuclear factor-erythroid 2 related factor 2 (Nrf2), and nuclear factor kappa B (NF-κB)) [109,110,111],”
  • Stable HepG2 panels with overexpression of individual CYPs have demonstrated suitability for identifying metabolically mediated toxicity and for determining the contribution of a specific isoform to the biotransformation of a xenobiotic.

    “Stable HepG2 panels with overexpression of individual CYPs have already demonstrated their suitability for identifying metabolically mediated toxicity and for determining the contribution of a specific isoform to the biotransformation of a xenobiotic [112,113].”

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Authors
Xuan, J., Chen, S., Ning, B., Tolleson, W. H., & Guo, L.
Affiliations
National Center for Toxicological Research (US)
Corresponding author
Guo, Lei
Venue
Chemico-Biological Interactions
Publisher
Elsevier BV
Published
2016-08
Volume
255
Pages
63-73
ISSN
0009-2797 (ISSN-L)
OpenAlex
W1773543011
Cited by
103
References
3
Citations by year
2026: 7 · 2025: 12 · 2024: 15 · 2023: 7 · 2022: 9 · 2021: 10 · 2020: 12 · 2019: 7 · 2018: 7 · 2017: 6 · 2016: 11
FWCI
9.33
Type
journal article
Language
en
Open access
Locations
  • Chemico-Biological Interactions (acceptedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
  • OSTI OAI (U.S. Department of Energy Office of Scientific and Technical Information) (submittedVersion)
Funders
  • U.S. Department of Energy
  • Oak Ridge Institute for Science and Education
Topics
  • Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Pharmacology › Drug-Induced Hepatotoxicity and Protection
  • Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Pharmacology › Pharmacogenetics and Drug Metabolism
  • Health Sciences › Medicine › Oncology › Drug Transport and Resistance Mechanisms
Keywords
drug-induced liver injury, cytochrome P450, HepG2 cells, drug metabolism, reactive metabolites, amiodarone, chlorpromazine, primaquine, in vitro toxicity screening
MeSH terms
Amiodarone, Antimalarials, Cell Line, Chlorpromazine, Cytochrome P-450 Enzyme System, Drug Evaluation, Preclinical, Humans, Liver, Primaquine, RNA, Messenger, Antipsychotic Agents, Gene Expression, Protein Isoforms, Chemical and Drug Induced Liver Injury, Hep G2 Cells, Cytochrome P-450 Enzyme Inhibitors

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