2019
DOI: 10.1111/acer.14133
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Effects of Acute Ethanol Administration on Brain Oxidative Status: The Role of Acetaldehyde

Abstract: alez Arag on, and Mar ıa Muriach Background: Ethanol (EtOH), one of the most widely consumed substances of abuse, can induce brain damage and neurodegeneration. EtOH is centrally metabolized into acetaldehyde, which has been shown to be responsible for some of the neurophysiological and cellular effects of EtOH. Although some of the consequences of chronic EtOH administration on cell oxidative status have been described, the mechanisms by which acute EtOH administration affects the brain's cellular oxidative s… Show more

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Cited by 11 publications
(9 citation statements)
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References 85 publications
(113 reference statements)
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“…An important goal for future studies is to assess more accurate blood alcohol levels early in the operant session in both male and female rats while also taking into account the detrimental effects of alcohol metabolites in the brain (Baliño et al, 2019); reviewed in (Erol and Karpyak, 2015;Israel et al, 2015).…”
Section: Blood Alcohol Levelsmentioning
confidence: 99%
“…An important goal for future studies is to assess more accurate blood alcohol levels early in the operant session in both male and female rats while also taking into account the detrimental effects of alcohol metabolites in the brain (Baliño et al, 2019); reviewed in (Erol and Karpyak, 2015;Israel et al, 2015).…”
Section: Blood Alcohol Levelsmentioning
confidence: 99%
“…Oxidative metabolism of ethanol persuades ROS production and OS. Ethanol exposure causes membrane lipid peroxidation [ 54 ], depletion of glutathione, and formation of protein carbonyl that serve as markers of OS in the brain [ 55 ]. Several dopaminergic neurons are engaged in ethanol-related impairments in mammalian CNS as well as in Drosophila [ 56 ].…”
Section: Discussionmentioning
confidence: 99%
“…(1,5) The normal level of homeostasis of laboratory animals and humans is maintained at blood concentrations of EE of about 0.05-0.2 mM, and EA is about 0.3-0.8 μM. The biological role of EE is diverse: (1) is a high-energy compound and under normal conditions can provide up to 10% of the body's energy needs; (2) participates in the maintenance of the liquid-crystalline, fluid state of the lipid layer of membranes, "liquefying" (fluidizing) them; (11)(12)(13) (3) is a regulator of lipid peroxidation in cell membranes, showing properties of a free radical trap and activating cholesterol synthesis. (11) EA is chemically very active, does not penetrate cell membranes, but can change their permeability to other substances.…”
Section: Adh2mentioning
confidence: 99%
“…(2) regulatory modification (through the formation of Schiff bases) of opioid peptides; (3) with the participation of EA, endogenous morphine and morphine-like compounds are synthesized; (4) regulates the exchange of the most important neurochemical mediators of the amine nature: dopamine, norepinephrine, serotonin; hormone adrenaline. (12)(13)(14) Everything discussed above allows us to consider the EE-EA system as an important element of non-specific regulatory systems of the body, providing the body's adaptive capabilities to the effects of stress, including cold.…”
Section: Adh2mentioning
confidence: 99%
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