Related Experiment Video

Updated: Aug 17, 2026

Visualization of Mitochondrial Respiratory Function using Cytochrome C Oxidase / Succinate Dehydrogenase (COX/SDH) Double-labeling Histochemistry
06:53

Visualization of Mitochondrial Respiratory Function using Cytochrome C Oxidase / Succinate Dehydrogenase (COX/SDH) Double-labeling Histochemistry

Published on: November 23, 2011

Oxidation of mitochondrial proteins and DNA following administration of ethanol

P Wieland1, B H Lauterburg

  • 1Department of Clinical Pharmacology, University of Bern, Switzerland.

Biochemical and Biophysical Research Communications
|August 24, 1995
PubMed

Insights

Ethanol intake causes mitochondrial DNA oxidation in mice, leading to lasting damage. This study reveals how alcohol affects mitochondria, even after drinking stops.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Toxicology

Background:

  • Alcohol consumption is linked to mitochondrial dysfunction.
  • Mitochondrial abnormalities persist in alcoholics even after ethanol cessation.
  • Oxidative stress is a proposed mechanism for this damage.

Purpose of the Study:

  • To investigate the role of mitochondrial DNA oxidation in alcohol-induced mitochondrial damage.
  • To determine if ethanol directly causes oxidative damage to mitochondrial DNA.
  • To explore the relationship between glutathione levels and mitochondrial oxidative stress.

Main Methods:

  • Mice were administered ethanol (4g/kg).
  • Liver homogenates and mitochondria were isolated 3 hours post-administration.
  • Levels of glutathione (GSH), oxidized glutathione (GSSG), oxidized proteins, carbonyls, and 8-hydroxy-2'-deoxyguanosine (8-OHdG) in DNA were measured.
  • Glutathione depletion was induced using diethyl maleate.

Main Results:

  • Ethanol decreased liver homogenate GSH by 25% without increasing GSSG or oxidized proteins.
  • Mitochondria showed significantly increased carbonyl content and DNA oxidation (8-OHdG).
  • Diethyl maleate-induced GSH depletion selectively increased mitochondrial protein and DNA oxidation.

Conclusions:

  • Ethanol induces oxidative damage specifically in mitochondria, including to mitochondrial DNA.
  • Low glutathione levels exacerbate mitochondrial oxidative stress.
  • Combined effects of DNA oxidation, low GSH, and potentially impaired DNA repair may cause permanent mitochondrial damage in alcoholics.

More Related Videos

Ratiometric Biosensors that Measure Mitochondrial Redox State and ATP in Living Yeast Cells12:22

Ratiometric Biosensors that Measure Mitochondrial Redox State and ATP in Living Yeast Cells

Published on: July 22, 2013

Assessment of Glutamine as a Fuel Source for Alveolar Macrophages Exposed to Chronic Ethanol Using an Extracellular Flux Bioanalyzer08:37

Assessment of Glutamine as a Fuel Source for Alveolar Macrophages Exposed to Chronic Ethanol Using an Extracellular Flux Bioanalyzer

Published on: November 15, 2024

Related Concept Videos

Pyruvate Oxidation01:15

Pyruvate Oxidation

After glycolysis, the charged pyruvate molecules enter the mitochondria via active transport and undergo three enzymatic reactions. These reactions ensure that pyruvate can enter the next metabolic pathway so that energy stored in the pyruvate molecules can be harnessed by the cells.
First, the enzyme pyruvate dehydrogenase removes the carboxyl group from pyruvate and releases it as carbon dioxide. The stripped molecule is then oxidized and releases electrons, which are then picked up by NAD+...
Autoxidation of Ethers to Peroxides and Hydroperoxides02:23

Autoxidation of Ethers to Peroxides and Hydroperoxides

Ethers represent a class of chemical compounds that become more dangerous with prolonged storage because they tend to form explosive peroxides when standing in the air. Autoxidation is the spontaneous oxidation of a compound in air. In the presence of oxygen, ethers slowly oxidize to form hydroperoxides and dialkyl peroxides.
Electron Transport Chain: Complex I and II01:46

Electron Transport Chain: Complex I and II

The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
ROS generation is regulated and maintained at moderate levels necessary...
The Electron Transport Chain01:30

The Electron Transport Chain

The electron transport chain or oxidative phosphorylation is an exothermic process in which free energy released during electron transfer reactions is coupled to ATP synthesis. This process is a significant source of energy in aerobic cells, and therefore inhibitors of the electron transport chain can be detrimental to the cell's metabolic processes.
Inhibitors of the electron transport chain
Rotenone, a widely used pesticide, prevents electron transfer from Fe-S cluster to ubiquinone or Q in...
Oxidation of Alcohols02:37

Oxidation of Alcohols

In this lesson, the oxidation of alcohols is discussed in depth. The various reagents used for oxidation of primary and secondary alcohols are detailed, and their mechanism of action is provided.
The process of oxidation in a chemical reaction is observed in any of the three forms:
Bioactivation and Tissue Toxicity01:25

Bioactivation and Tissue Toxicity

Bioactivation is a metabolic process that transforms less reactive substances into highly reactive metabolites, initiating tissue toxicity. This transformation can lead to various toxic effects, including carcinogenesis and teratogenesis. Reactive metabolites are classified into two main types: electrophiles and free radicals.Electrophiles are electron-deficient species and are produced primarily by the enzyme cytochrome P-450 during the metabolism of compounds containing carbon, nitrogen, or...