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Ethanol‐Induced Oxygen Radical Formation and Lipid Peroxidation in Rat Brain: Effect of Chronic Alcohol Consumption
Abstract
Abstract: The effect of chronic and in vitro ethanol exposure on brain oxygen radical formation and lipid peroxidation was analyzed. Ethanol induces a dose‐dependent increase in lipid peroxidation in brain homogenates. The peroxidative effects of alcohol seem to be related to both cytochrome P450 and the ethanol‐inducible form of cytochrome P450 (CYP2E1), because preincubation with metyrapone (an inhibitor of cytochrome P450) or with an antibody against CYP2E1 abolished the ethanol‐increased lipid peroxidation. Using the formation of dichlorofluorescein, we also demonstrated that both in vitro and chronic alcohol exposure significantly enhanced the formation of oxygen radical species in synaptosomes. Chronic alcohol treatment also leads to an induction of cytochrome P450 (230%), NADPH cytochrome c reductase (180%), NADPH oxidation (184%), and CYP2E1 in brain microsomes. In addition, this treatment produced a decrease in the GSH/GSSG ratio in brain and significantly enhanced the levels of superoxide dismutase and catalase activities. This mechanism could be involved in the toxic effects of ethanol on brain and membrane alterations occurring after chronic ethanol intake.
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“In contrast, CYP2E1 is widely expressed throughout the brain, such as in the cerebral cortex, hippocampus, and cerebellum.”
From Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury (2021) · cites this paper as [155]
In the citing paper
“The role of CYP2E1 in brain ethanol metabolism and its association with alcohol-mediated oxidative neuronal injury155–160 and aging-related AD and PD161 have also been suggested.”
From Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury (2021) · cites this paper as [155]
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Roles of Oxidative Stress and Autophagy in Alcohol-Mediated Brain Damage
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“However, it is important to consider the potential impacts of the elevated CYP2E1 on the oxidative cell and brain injury, since CYP2E1 was shown to be induced by 17.5 mM ethanol in primary neuronal cells [61], primary astrocytes [62], and rodent brains after chronic alcohol exposures [63–66].”
InfluentialImmune function genes, genetics, and the neurobiology of addiction
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Alpha-lipoic acid prevents ethanol-induced protein oxidation in mouse hippocampal HT22 cells
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Ethanol Induced Changes in Superoxide Anion and Nitric Oxide in Cultured Microglia
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Changes in some pro-and antioxidants in rat cerebellum after chronic alcohol intake
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“It appears that ethanol-induced neurotoxicity is mediated by oxidative stress and mitochondrial malfunction [11, 13, 25].”
Background
Metadata
- Authors
- Montoliu, C., Vallés, S., Renau‐Piqueras, J., & Guerri, C.
- Affiliations
- Instituto de Investigación Sanitaria La Fe (ES)
- Corresponding author
- Guerri, Consuelo
- Venue
- Journal of Neurochemistry
- Publisher
- Wiley
- Published
- 1994-11
- Volume
- 63
- Issue
- 5
- Pages
- 1855-1862
- ISSN
- 0022-3042 (ISSN-L)
- 1471-4159
- OpenAlex
- W1978987336
- Cited by
- 269
- References
- 0
- Citations by year
- 2026: 2 · 2025: 2 · 2024: 2 · 2023: 3 · 2022: 5 · 2021: 4 · 2020: 1 · 2019: 7 · 2018: 10 · 2017: 6 · 2016: 9 · 2015: 10 · 2014: 10 · 2013: 5 · 2012: 13
- FWCI
- 6.86
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Neurochemistry (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Biochemistry (medical) › Antioxidant Activity and Oxidative Stress
- Health Sciences › Medicine › Pathology and Forensic Medicine › Alcohol Consumption and Health Effects
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Keywords
- chronic alcohol consumption, oxygen free radicals, lipid peroxidation, brain, cytochrome P450, CYP2E1, metyrapone, dichlorofluorescein, synaptosomes, NADPH-cytochrome c reductase, NADPH oxidation, glutathione, superoxide dismutase, catalase, ethanol neurotoxicity, brain microsomes
- MeSH terms
- Ethanol, Alcoholism, Animals, Brain, Brain Chemistry, Catalase, Cytochrome P-450 Enzyme System, Dose-Response Relationship, Drug, Electrophoresis, Polyacrylamide Gel, Female, Free Radicals, Glutathione, Isomerism, NADP, Oxygen, Superoxide Dismutase, Synaptosomes, Immunoblotting, Lipid Peroxidation, Rats, Wistar, Reactive Oxygen Species, Glutathione Disulfide, Rats
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