ArticlePloS one2014
Acute ethanol causes hepatic mitochondrial depolarization in mice: role of ethanol metabolism.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 73 citations in OpenAlex.
- A preclinical candidate of cyclophilin D inhibition improves alcohol-associated liver injury.Cell reports. Medicine · 2026Article
- Zonal hepatocellular responses to acute ethanol consumption: impacts on mitochondrial function and liver metabolism.Toxicological sciences : an official journal of the Society of Toxicology · 2026Article
- Role of Acetaldehyde and Dysregulated Mitophagic Lysosomal Processing in Chronic-Binge Ethanol-Induced Liver Injury.International journal of molecular sciences · 2025Article
- Synergistic toxicity in alcohol-associated liver disease and PFAS exposure.Toxicological sciences : an official journal of the Society of Toxicology · 2025Review
- Autobrewery Syndrome and Endogenous Ethanol Production in Patients with MASLD: A Perspective from Chronic Liver Disease.International journal of molecular sciences · 2025Review
- MitoTracker Red for isolation of zone-specific hepatocytes and characterization of hepatic sublobular metabolism.Biochemical and biophysical research communications · 2024Article
- Transgenic expression of human cytochrome P450 2E1 in C. elegans and rat PC-12 cells sensitizes to ethanol-induced locomotor and mitochondrial effects.Biochemical and biophysical research communications · 2024Article
- Article
- The mitophagy pathway and its implications in human diseases.Signal transduction and targeted therapy · 2023Review
- Pathogenesis of Alcoholic Fatty Liver a Narrative Review.Life (Basel, Switzerland) · 2023Review
- LP342, a novel histone deacetylase inhibitor, decreases nitro-oxidative stress, mitochondrial dysfunction and hepatic ischaemia/reperfusion injury in mice.RPS pharmacy and pharmacology reports · 2023Article
- A Meta-Analysis of Preclinical Studies to Investigate the Effect ofAntioxidants (Basel, Switzerland) · 2023Review
- Mitochondrial depolarization after acute ethanol treatment drives mitophagy in living mice.Autophagy · 2022Article
- Quercetin Protects Ethanol-Induced Hepatocyte Pyroptosis via Scavenging Mitochondrial ROS and Promoting PGC-1Oxidative medicine and cellular longevity · 2022Article
- In vivo protective effect against ethanol metabolism and liver injury of oyster (Food science and biotechnology · 2021Article
- Mitophagy in Human Diseases.International journal of molecular sciences · 2021Review
- Ibuprofen Increases the Hepatotoxicity of Ethanol through Potentiating Oxidative Stress.Biomolecules & therapeutics · 2021Article
- Mitochondrial dysfunction and liver disease: role, relevance, and potential for therapeutic modulation.Therapeutic advances in gastroenterology · 2021Review
- Cell Death and Liver Disease.Gut and liver · 2020Review
- Autophagy mitigates ethanol-induced mitochondrial dysfunction and oxidative stress in esophageal keratinocytes.PloS one · 2020Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
BACKGROUND/
aimsAn increase of ethanol metabolism and hepatic mitochondrial respiration occurs in vivo after a single binge of alcohol. Here, our aim was to determine how ethanol intake affects hepatic mitochondrial polarization status in vivo in relation to ethanol metabolism and steatosis.
methodsHepatic mitochondrial polarization, permeability transition (MPT), and reduce pyridine nucleotides, and steatosis in mice were monitored by intravital confocal/multiphoton microscopy of the fluorescence of rhodamine 123 (Rh123), calcein, NAD(P)H, and BODIPY493/503, respectively, after gavage with ethanol (1-6 g/kg).
resultsMitochondria depolarized in an all-or-nothing fashion in individual hepatocytes as early as 1 h after alcohol. Depolarization was dose- and time-dependent, peaked after 6 to 12 h and maximally affected 94% of hepatocytes. This mitochondrial depolarization was not due to onset of the MPT. After 24 h, mitochondria of most hepatocytes recovered normal polarization and were indistinguishable from untreated after 7 days. Cell death monitored by propidium iodide staining, histology and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) was low throughout. After alcohol, mitochondrial NAD(P)H autofluorescence increased and decreased, respectively, in hepatocytes with polarized and depolarized mitochondria. Ethanol also caused steatosis mainly in hepatocytes with depolarized mitochondria. Depolarization was linked to ethanol metabolism, since deficiency of alcohol dehydrogenase and cytochrome-P450 2E1 (CYP2E1), the major ethanol-metabolizing enzymes, decreased mitochondrial depolarization by ∼ 70% and ∼ 20%, respectively. Activation of aldehyde dehydrogenase decreased depolarization, whereas inhibition of aldehyde dehydrogenase enhanced depolarization. Activation of aldehyde dehydrogenase also markedly decreased steatosis.
conclusionsAcute ethanol causes reversible hepatic mitochondrial depolarization in vivo that may contribute to steatosis and increased mitochondrial respiration. Onset of this mitochondrial depolarization is linked, at least in part, to metabolism of ethanol to acetaldehyde.
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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.