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

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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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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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Central role of mitochondria in drug-induced liver injury

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