Current View on the Mechanisms of Alcohol-Mediated Toxicity

Birková, Anna; Hubková, Beáta; Čižmárová, Beáta; Bolerázska, Beáta

doi:10.3390/ijms22189686

Cited by 29 publications

(31 citation statements)

References 157 publications

(203 reference statements)

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“…Excessive consumption can cause neuropathological symptoms [ 67 ], cardiovascular diseases [ 68 ], liver diseases [ 69 ], intestinal diseases [ 70 ], liver cancers [ 71 ], and infectious diseases due to the weakened immune system of the body [ 72 ]. The main component of alcoholic drinks is ethanol, which has shown to exert oxidative damages to biological macromolecules via acetaldehyde-DNA/RNA/protein adduct formation, thereby drastically inducing cellular ROS production and systemic OS [ 14 , 19 , 22 ]. These toxic conditions can then lead to abrupt changes in the levels of antioxidant enzymes and other forms of antioxidant molecules in the body.…”

Section: Discussionmentioning

confidence: 99%

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The Status of Oxidative Stress in Patients with Alcohol Dependence: A Meta-Analysis

Zhou

Tan

et al. 2022

Antioxidants

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Alcohol-induced oxidative stress (OS) plays a pivotal role in the pathophysiology of alcohol dependence (AD). This meta-analysis was aimed at investigating the changes in the levels of OS biomarkers in AD patients. We included relevant literature published before 1 April 2022, from the PubMed, Web of Science, and EBSCO databases following PRISMA guidelines. Finally, 15 eligible articles were enrolled in this meta-analysis, including 860 patients and 849 controls. Compared with healthy controls, AD patients had lower activities of superoxide dismutase (SOD) and glutathione peroxidase (GPx) enzymes, and lower levels of albumin, while levels of malondialdehyde (MDA), vitamin B12, homocysteine, and bilirubin were significantly increased in serum/plasma samples of AD subjects (all p < 0.05). In male patients, the activities of SOD and GPx were increased in serum/plasma but decreased in erythrocytes (all p < 0.05). The opposite trends in the level of SOD and GPx activities in serum/plasma and erythrocytes of male patients could be used as the biomarker of alcohol-induced OS injury, and the synergistic changes of MDA, vitamin B12, albumin, bilirubin, and homocysteine levels should also be considered.

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Section: Discussionmentioning

confidence: 99%

“…In the brain, ethanol is oxidized to acetaldehyde through the action of catalases (CATs) [ 15 , 16 ], cytochrome P450 enzymes (CYP2E1) [ 17 ], and alcohol dehydrogenase (ADH) [ 18 , 19 ]. Notably, CAT and CYP2E1 play major roles in catalyzing the biochemical conversion of ethanol to acetaldehyde [ 20 ].…”

Section: Introductionmentioning

confidence: 99%

The Status of Oxidative Stress in Patients with Alcohol Dependence: A Meta-Analysis

Zhou

Tan

et al. 2022

Antioxidants

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“…Introduction. Enhancement of free radical oxidation and the development of oxidative stress is the main pathogenetic mechanism of ethanol toxicity [1]. Ethanolinduced oxidative stress is the result of combined impairment of antioxidant defense and the production of reactive oxygen species by mitochondrial electron transport chain, alcohol-inducible cytochrome P450 (CYP) 2E1 and activated phagocytes.…”

Section: висновки уведення мелатоніну зменшує токсичні ефекти у щурів...mentioning

confidence: 99%

“…Ethanolinduced oxidative stress is the result of combined impairment of antioxidant defense and the production of reactive oxygen species by mitochondrial electron transport chain, alcohol-inducible cytochrome P450 (CYP) 2E1 and activated phagocytes. The glutathione system plays an important role in antiradical and antiperoxide protection of cells [1,2]. The coordinated action of all its components (reduced glutathione, glutathione peroxidase, glutathione-S-transferase, glutathione reductase) helps to maintain the optimal level of redox potential in cells [3].…”

Section: висновки уведення мелатоніну зменшує токсичні ефекти у щурів...mentioning

confidence: 99%

The glutathione system state in rats exposed to ethanol intoxication, its combination with caffeine and modified photoperiod

2022

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Objective. To study the content of reduced glutathione (GSH), activities of glutathione peroxidase (GP) and glutathione-S-transferase enzymes (GST) in blood and liver of rats exposed to subacute alcohol intoxication, its combination with caffeine intake or constant light exposure, and the possibility of their correction with melatonin.Materials and methods. Experiments were performed on 42 male rats weighing 180-200 g kept under standard conditions of the vivarium and artificial equinox. Alcohol intoxication was induced by intragastric administration 40 % ethanol at a dose of 7 ml/kg of body weight for 7 days. Caffeine was administered by gavage at a dose of 30 mg/kg of body weight.Results. Ethanol poisoning and its combination with caffeine intake or exposure to constant light resulted in a decrease in GSH level and GP activity in RBCs and liver, besides the combination of ethanol+light resulted in more pronounced depletion of the parameters. The combination of ethanol with caffeine resulted in less reduction of GSH level in the blood (by 25%) but more depletion of GSH in the liver (by 45% vs. control) than in ethanol-treated rats. There was an elevation of GST activity in the liver of all groups of alcoholized animals. Administration of 5 mg/kg melatonin for 7 days limited depletion in GSH and prevented the changes in GP and GST activities in the blood and liver of all groups of animals.Conclusions. Melatonin administration prevented ethanol-induced toxicity in rats exposed to ethanol and its combination with caffeine or constant light for 7 days by limiting the depletion in GSH and preventing the changes in GP and GST activities in the blood and liver of all groups of animals.

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“…Ethanol detoxifi cation occurs mainly in the liver by alcohol dehydrogenase, catalase, and microsomal monooxygenase system yielding acetaldehyde. Acetaldehyde mediates an increase in nitrogen and oxygen reactive species, activation of free radical oxidation of unsaturated fatty acids, proteins, nucleic acids, depletion of antioxidants, which defi nes the concept of oxidative stress and leads to irreversible macromolecular changes in cells [1]. Another important source of ROS is cytochrome P450 2E1 (CYP2E1) which expression is induced by ethanol intake.…”

Section: Introductionmentioning

confidence: 99%

Melatonin Prevents Oxidative Stress in Rats Exposed to Ethanol Intoxication, Its Combination With Caffeine and Light Exposure

Davydova¹,

Hryhorieva²

2022

Clin. and experim. pathol.

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The аim of the research – to investigate the effects of melatonin on oxidative stressbiomarkers malonic dialdehyde (MDA) and oxidatively modified proteins (OMP) inblood, liver and kidneys of rats exposed to subacute alcohol intoxication, its combinationwith constant light exposure, and caffeine intake.Materials and methods. Experiments were performed on 42 male rats weighing180-200 g kept under standard conditions of vivarium and artificial equinox. Subacutealcohol intoxication was induced by intragastric administration of 40 % ethanol at a doseof 7 ml/kg of body weight for 7 days. Caffeine was administered by gavage at a doseof 30 mg/kg of body weight.Results. Ethanol poisoning results in increase in MDA and OMB, and liver was the mostaffected (90 % and 42 % higher than control). The combination of ethanol with caffeinereduced the intensity of oxidative stress in the blood but increased the toxic effectsof ethanol on the liver (MDA and OMP were 116 % and 60 % above control range).The most significant increase in MDA was in the liver and kidneys under combinationof alcohol intoxication with exposure to constant light (139 % and 33 % respectively).There was a decrease in OMB level along with elevation of MDA level in kidneys of allgroups of alcoholized animals.Administration of 5 mg/kg melatonin for 7 days limited the rise in MDA in the bloodand liver of animals and changes in OMB content in the blood liver and kidneys of animalsexposed to ethanol and constant lighting. Melatonin showed to be less effective in theliver and kidneys of rats treated with a combination of ethanol and caffeine.Conclusion. The data obtained are evidence of the pronounced antioxidant melatoninaction and its capacity to prevent toxic effects of ethanol and its combination withconstant lighting and caffeine introduction into organism.

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Current View on the Mechanisms of Alcohol-Mediated Toxicity

Cited by 29 publications

References 157 publications

The Status of Oxidative Stress in Patients with Alcohol Dependence: A Meta-Analysis

The Status of Oxidative Stress in Patients with Alcohol Dependence: A Meta-Analysis

The glutathione system state in rats exposed to ethanol intoxication, its combination with caffeine and modified photoperiod

Melatonin Prevents Oxidative Stress in Rats Exposed to Ethanol Intoxication, Its Combination With Caffeine and Light Exposure

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