Central role of mitochondria in drug-induced liver injury

Pessayre, Dominique; Fromenty, Bernard; Berson, Alain; Robin, Marie-Anne; Lettéron, Philippe; Moreau, Richard; Mansouri, Abdellah

doi:10.3109/03602532.2011.604086

Cited by 277Drug-Induced Hepatotoxicity and ProtectionMitochondrial Function and PathologyLiver physiology and pathology

Central role of mitochondria in drug-induced liver injury

Pessayre, Dominique, Fromenty, Bernard, Berson, Alain, Robin, Marie-Anne, Lettéron, Philippe, Moreau, Richard, Mansouri, Abdellah·2012·Drug Metabolism Reviews

DOI 10.3109/03602532.2011.604086

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Abstract

A frequent mechanism for drug-induced liver injury (DILI) is the formation of reactive metabolites that trigger hepatitis through direct toxicity or immune reactions. Both events cause mitochondrial membrane disruption. Genetic or acquired factors predispose to metabolite-mediated hepatitis by increasing the formation of the reactive metabolite, decreasing its detoxification, or by the presence of critical human leukocyte antigen molecule(s). In other instances, the parent drug itself triggers mitochondrial membrane disruption or inhibits mitochondrial function through different mechanisms. Drugs can sequester coenzyme A or can inhibit mitochondrial β-oxidation enzymes, the transfer of electrons along the respiratory chain, or adenosine triphosphate (ATP) synthase. Drugs can also destroy mitochondrial DNA, inhibit its replication, decrease mitochondrial transcripts, or hamper mitochondrial protein synthesis. Quite often, a single drug has many different effects on mitochondrial function. A severe impairment of oxidative phosphorylation decreases hepatic ATP, leading to cell dysfunction or necrosis; it can also secondarily inhibit ß-oxidation, thus causing steatosis, and can also inhibit pyruvate catabolism, leading to lactic acidosis. A severe impairment of β-oxidation can cause a fatty liver; further, decreased gluconeogenesis and increased utilization of glucose to compensate for the inability to oxidize fatty acids, together with the mitochondrial toxicity of accumulated free fatty acids and lipid peroxidation products, may impair energy production, possibly leading to coma and death. Susceptibility to parent drug-mediated mitochondrial dysfunction can be increased by factors impairing the removal of the toxic parent compound or by the presence of other medical condition(s) impairing mitochondrial function. New drug molecules should be screened for possible mitochondrial effects.

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Chronic and/or binge alcohol, high fat diets, tobacco smoking, or certain hepatotoxic drugs can directly damage the mitochondrial ETC, producing greater amounts of ROS leaked from the ETS.
“However, chronic and/or binge alcohol, high fat diets, tobacco smoking, or certain hepatotoxic drugs can directly damage the mitochondrial ETC, producing greater amounts of ROS leaked from the ETS [24], [25], [26], [27].”
From Mitochondrial dysfunction and tissue injury by alcohol, high fat, nonalcoholic substances and pathological conditions through post-translational protein modifications (2014) · cites this paper as [24]

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Mitochondrial Dysfunction and Signaling in Chronic Liver Diseases
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Animal models of drug-induced liver injury
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Aflatoxin B1 impairs mitochondrial functions, activates ROS generation, induces apoptosis and involves Nrf2 signal pathway in primary broiler hepatocytes
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Mitochondrial Roles and Cytoprotection in Chronic Liver Injury
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Drug-Induced Steatohepatitis
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Betaine treatment protects liver through regulating mitochondrial function and counteracting oxidative stress in acute and chronic animal models of hepatic injury
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“Furthermore, these protein adducts can serve as a neo-antigen of hapten–carrier conjugate proteins to activate immune responses and to facilitate infiltration of neutrophils into the liver to promote inflammation [18–21,24,166–168].”
BackgroundInfluential
A high content screening assay to predict human drug-induced liver injury during drug discovery
Persson, M., Løye, A. F., Mow, T. J., & Hornberg, J. J. (2013) · Journal of Pharmacological and Toxicological Methods · doi:10.1016/j.vascn.2013.08.001 · Cited by 119 · see citing works
Molecular insights into the role of mitochondria in non-alcoholic fatty liver disease
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Mitochondrial–Lysosomal Axis in Acetaminophen Hepatotoxicity
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Mechanistic review of drug-induced steatohepatitis
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Low Dose Acetaminophen Induces Reversible Mitochondrial Dysfunction Associated with Transient c-Jun N-Terminal Kinase Activation in Mouse Liver
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AMPK Activation Prevents and Reverses Drug-Induced Mitochondrial and Hepatocyte Injury by Promoting Mitochondrial Fusion and Function
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The Importance of Patient-Specific Factors for Hepatic Drug Response and Toxicity
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Crocin, a dietary colorant mitigates cyclophosphamide-induced organ toxicity by modulating antioxidant status and inflammatory cytokines
Jnaneshwari, S., Hemshekhar, M., Santhosh, M. S., Sunitha, K., Thushara, R. M., Thirunavukkarasu, C., Kemparaju, K., & Girish, K. S. (2013) · Journal of Pharmacy and Pharmacology · doi:10.1111/jphp.12016 · Cited by 88 · see citing works
Metabolic activation and drug‐induced liver injury: in vitro approaches for the safety risk assessment of new drugs
Gómez‐Lechón, M. J., Tolosa, L., & Donato, M. T. (2015) · Journal of Applied Toxicology · doi:10.1002/jat.3277 · Cited by 87 · see citing works
Mitochondrial toxicity of diclofenac and its metabolites via inhibition of oxidative phosphorylation (ATP synthesis) in rat liver mitochondria: Possible role in drug induced liver injury (DILI)
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Calcium Signaling in Liver Injury and Regeneration
Oliva‐Vilarnau, N., Hankeová, S., Vorrink, S. U., Mkrtchian, S., Andersson, E. R., & Lauschke, V. M. (2018) · Frontiers in Medicine · doi:10.3389/fmed.2018.00192 · Cited by 84 · see citing works
Role of non-steroidal anti-inflammatory drugs on intestinal permeability and nonalcoholic fatty liver disease
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Busting the myth of methotrexate chronic hepatotoxicity
Martino, V. D., Weil, D., Verhoeven, F., Aubin, F., Avouac, J., Vuitton, L., Lioté, F., Thévenot, T., & Wendling, D. (2022) · Nature Reviews Rheumatology · doi:10.1038/s41584-022-00883-4 · Cited by 83 · see citing works
Fasiglifam (TAK-875): Mechanistic Investigation and Retrospective Identification of Hazards for Drug Induced Liver Injury
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Agonism of the 5-Hydroxytryptamine 1F Receptor Promotes Mitochondrial Biogenesis and Recovery from Acute Kidney Injury
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Contamination of Aflatoxins Induces Severe Hepatotoxicity Through Multiple Mechanisms
Hua, Z., Liu, R., Chen, Y., Liu, G., Li, C., Song, Y., Cao, Z., Li, W., Lu, C. C., Lu, C. C., et al. (2021) · Frontiers in Pharmacology · doi:10.3389/fphar.2020.605823 · Cited by 78 · see citing works
Effects of aflatoxin B1 on mitochondrial respiration, ROS generation and apoptosis in broiler cardiomyocytes
Wang, W., Xu, Z., Yu, C., & Xu, X. (2017) · Animal Science Journal · doi:10.1111/asj.12796 · Cited by 76 · see citing works
Mitochondrial depolarization after acute ethanol treatment drives mitophagy in living mice
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Treatment of acetaminophen-induced liver injury with exogenous mitochondria in mice
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Authors: Pessayre, D., Fromenty, B., Berson, A., Robin, M.-A., Lettéron, P., Moreau, R., & Mansouri, A.
Affiliations: Inserm (FR)
Corresponding author: Pessayre, Dominique
ORCID: Fromenty, Bernard
Moreau, Richard
Mansouri, Abdellah
Venue: Drug Metabolism Reviews
Publisher: Informa UK Limited
Published: 2012-01-30
Volume: 44
Issue: 1
Pages: 34-87
ISSN: 0360-2532 (ISSN-L)
1097-9883
DOI: 10.3109/03602532.2011.604086
OpenAlex: W2076781542
Cited by: 277
References: 604
Citations by year: 2026: 13 · 2025: 17 · 2024: 11 · 2023: 21 · 2022: 22 · 2021: 31 · 2020: 16 · 2019: 15 · 2018: 26 · 2017: 19 · 2016: 21 · 2015: 26 · 2014: 23 · 2013: 13 · 2012: 2
FWCI: 1.75
Type: journal article
Language: en
Open access: closed
Locations: Drug Metabolism Reviews (publishedVersion)
PubMed (publishedVersion)
HAL (submittedVersion)
Topics: Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Pharmacology › Drug-Induced Hepatotoxicity and Protection
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
Health Sciences › Medicine › Hepatology › Liver physiology and pathology
Keywords: drug-induced liver injury, mitochondrial dysfunction, reactive drug metabolites, mitochondrial membrane disruption, oxidative phosphorylation, ATP synthase inhibition, mitochondrial DNA damage, lactic acidosis, hepatic steatosis, steatosis, lipid peroxidation, human leukocyte antigen, genetic susceptibility, drug safety testing
MeSH terms: DNA, Mitochondrial, Pharmaceutical Preparations, Fatty Liver, Humans, Immune System, Liver, Mitochondria, Liver, Oxidation-Reduction, Reactive Oxygen Species, Cell Respiration, Mitochondrial Proteins, Chemical and Drug Induced Liver Injury, Drug-Related Side Effects and Adverse Reactions

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