ArticleToxicology in vitro : an international journal published in association with BIBRA2019
Differential toxic effects of bile acid mixtures in isolated mitochondria and physiologically relevant HepaRG cells.
Article in Toxicology in vitro : an international journal published in association with BIBRA, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 25 citations in OpenAlex.
- Investigation of Prophylactic and Therapeutic Effects of Boric Acid in an Experimental Mechanical Biliary Obstructive Cholestasis Rat Model.Biological trace element research · 2026Article
- In Vitro-In Silico Models to Elucidate Mechanisms of Bile Acid Disposition and Cellular Aerobics in Human Hepatocytes.The AAPS journal · 2025Article
- Bile Acids as Inducers of Protonophore and Ionophore Permeability of Biological and Artificial Membranes.Membranes · 2023Review
- Role of Hepatocyte Transporters in Drug-Induced Liver Injury (DILI)-In Vitro Testing.Pharmaceutics · 2022Review
- Bile Acids Induce Alterations in Mitochondrial Function in Skeletal Muscle Fibers.Antioxidants (Basel, Switzerland) · 2022Article
- 18β-Glycyrrhetinic Acid Protects against Cholestatic Liver Injury in Bile Duct-Ligated Rats.Antioxidants (Basel, Switzerland) · 2022Article
- Hepatoprotective Effects of Glycyrrhetinic Acid on Lithocholic Acid-Induced Cholestatic Liver Injury Through Choleretic and Anti-Inflammatory Mechanisms.Frontiers in pharmacology · 2022Article
- Dietary pectin caused great changes in bile acid profiles of Pelteobagrus fulvidraco.Fish physiology and biochemistry · 2021Article
- Article
- Prospect ofFrontiers in toxicology · 2021Review
- Redox-Dependent Effects in the Physiopathological Role of Bile Acids.Oxidative medicine and cellular longevity · 2021Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Bile acids (BAs) are recognised as the causative agents of toxicity in drug-induced cholestasis (DIC). Research in isolated mitochondria and HepG2 cells have demonstrated BA-mediated mitochondrial dysfunction as a key mechanism of toxicity in DIC. However, HepG2 cells are of limited suitability for DIC studies as they do not express the necessary physiological characteristics. In this study, the mitotoxic potentials of BA mixtures were assessed in isolated mitochondria and a better-suited hepatic model, HepaRG cells. BAs induced structural alterations and a loss of mitochondrial membrane potential (MMP) in isolated mitochondria however, this toxicity did not translate to HepaRG cells. There were no changes in oxygen consumption rate, MMP or ATP levels in glucose and galactose media, indicating that there was no direct mitochondrial toxicity mediated via electron transport chain dysfunction in HepaRG cells. Assessment of key biliary transporters revealed that there was a time-dependent reduction in the expression and activity of multi-drug resistance protein 2 (MRP2), which was consistent with the induction of cytotoxicity in HepaRG cells. Overall, the findings from this study have demonstrated that mitochondrial dysfunction is not a mechanism of BA-induced toxicity in HepaRG cells.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.