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Central role of mitochondria in drug-induced liver injury
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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“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].”
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Self-citation
Metadata
- Authors
- Pessayre, D., Fromenty, B., Berson, A., Robin, M.-A., Lettéron, P., Moreau, R., & Mansouri, A.
- Affiliations
- Inserm (FR)
- Corresponding author
- Pessayre, Dominique
- 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
- 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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