Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Hepatotoxicity due to mitochondrial dysfunction.

D Pessayre1, A Mansouri, D Haouzi

  • 1INSERM U481 and Centre de Recherche sur les Hépatites Virales de l'Association Claude Bernard, Hôpital Beaujon, Clichy, France. pessayre@bichat.inserm.fr

Cell Biology and Toxicology
|May 16, 2000
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Acute presentation of cocoon abdomen as intestinal obstruction mimicking with strangulated eventration: A case report.

International journal of surgery case reports·2024
Same author

[Ultrawide-field fundus photography showing frosted branch angiitis].

Journal francais d'ophtalmologie·2024
Same author

Roadmap to DILI research in Europe. A proposal from COST action ProEuroDILINet.

Pharmacological research·2023
Same author

3D multi-cell-type liver organoids: A new model of non-alcoholic fatty liver disease for drug safety assessments.

Toxicology in vitro : an international journal published in association with BIBRA·2023
Same author

Clinophobia: Dermatologists on the front line (16 cases).

Annales de dermatologie et de venereologie·2021
Same author

WITHDRAWN: Incidence and mortality of COVID-19 in Iranian multiple sclerosis patients treated with disease-modifying therapies.

Revue neurologique·2020

Mitochondrial dysfunction is a key factor in drug-induced liver disease, particularly microvesicular steatosis. Impaired beta-oxidation and reactive oxygen species production contribute to liver injury and nonalcoholic steatohepatitis.

Area of Science:

  • Hepatology
  • Mitochondrial Biology
  • Toxicology

Background:

  • Mitochondria are crucial for cellular energy production via fatty acid beta-oxidation, the tricarboxylic acid cycle, and oxidative phosphorylation.
  • They are also a primary source of reactive oxygen species (ROS) and play a role in programmed cell death.
  • Mitochondrial dysfunction is increasingly recognized as a significant mechanism in drug-induced liver injury (DILI).

Purpose of the Study:

  • To explore the role of mitochondrial dysfunction in the pathogenesis of drug-induced liver disease.
  • To elucidate the mechanisms by which mitochondrial damage leads to various forms of liver injury, including steatosis and steatohepatitis.

Main Methods:

  • Review of existing literature on mitochondrial function and drug-induced liver injury.

Related Experiment Videos

  • Analysis of pathways involved in fatty acid metabolism, oxidative stress, and hepatocyte cell death.
  • Correlation of mitochondrial defects with specific liver pathologies like microvesicular steatosis and nonalcoholic steatohepatitis.

    • Main Results:

    • Severe impairment of mitochondrial beta-oxidation leads to microvesicular steatosis, potentially causing liver failure.
    • Inhibition of beta-oxidation by endogenous or exogenous factors can trigger this condition.
    • Chronic mitochondrial dysfunction, including impaired beta-oxidation and increased ROS, drives nonalcoholic steatohepatitis, leading to lipid peroxidation and diverse liver lesions.
    • Mitochondrial permeability transition pore opening contributes to drug-induced cytolytic hepatitis, resulting in apoptosis or necrosis.

    Conclusions:

    • Mitochondrial dysfunction is a central mechanism in drug-induced liver disease, manifesting as steatosis and steatohepatitis.
    • Disruption of mitochondrial beta-oxidation and increased oxidative stress are key contributors to liver injury.
    • Understanding these mitochondrial pathways is critical for diagnosing and managing drug-induced liver conditions.