2020, Number 2
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ABSTRACTAlcoholism is a chronic disease that leads to behavioral problems that last during withdrawal. The consumption of ethanol increases the accumulation of Acetaldehyde and Reactive Oxygen Species causing damage to the brain. Two important neurotransmitters involved in neuronal damage are γ-Amino butyric acid (GABA) an inhibitory neurotransmitter and glutamate, the most important excitatory neurotransmitter. GABAergic receptor affections contribute to tolerance and dependence on ethanol and symptoms of hyperexcitability in the withdrawal while the affectations of the glutamatergic NMDA receptor contribute to tolerance and dependence on ethanol as well as to the establishment of withdrawal symptoms. The affectations in the metabolism of Ethanol trigger behavioral alterations since the dysfunction of the enzyme Acetaldehyde dehydrogenase causes accumulation at the brain level of Acetaldehyde, largely responsible for the brain damage caused during alcoholism. In this work, the existing experimental literature in databases such as PubMed and Medline is reviewed systematically and organized by subject, in logical order and starting from basic concepts, about the main elements in the relationship between oxidative stress and neuronal imbalance which form the basis of behavioral problems in the development of addiction and during withdrawal. Our objective is to contribute to clarify the existing knowledge about the relationships between certain biological factors (such as neurotransmitters and indicators of redox imbalance) and the effects of alcohol, highlighting the importance of some risk factors for the development of alcoholism.
Espert R, Gadea M. Neurobiología del alcoholismo. Bases bioquímicas y neurobiológicas de la adicción al alcohol. En: Monografía sobre el alcoholismo. Barcelona: Socidrogalcohol. 2012. p. 75-120. http://ibdigital.uib.es/ greenstone/collect/portal_social/index/assoc/socidrog/ alcohol0/004.dir/socidrogalcohol0004.pdf.
Climent B, Gago N, Llerena G, González V. Patología médica asociada al consumo perjudicial de alcohol. En: Monografía sobre el alcoholismo. Barcelona: Socidrogalcohol. 2012. p. 181-218. http://ibdigital. uib.es/greenstone/collect/portal_social/index/assoc/ socidrog/alcohol0/004.dir/socidrogalcohol0004.pdf.
Rehm JT, Shield KD, Rehm MX, Gmel G, Frick U. Alcohol consumption, alcohol dependence and attributable burden of disease in Europe. Potential gains from effective interventions for alcohol dependence. Toronto: Centre for Addiction and Mental Health (CAMH); 2012. Disponible en: http://amphoraproject. net/w2box/data/AMPHORAReports/CAMH_Alcohol_ Report_Europe_2012.pdf
Díaz-Soto M. T., Fraga Pérez A, Dranguet Vaillant J., Mallok A., Viebanh Hänsler R., Menéndez Cepero S, et al. Ozone Therapy Ameliorates Nervous System Disorders and Oxidative Stress in Patients During Ethanol Withdrawal-A Pilot Study. Ozone: Science & Engineering. 2012, 34: 432–437. https://doi.org/10.108 0/01919512.2012.717858.
Díaz-Soto M. T., Fraga Pérez A, Dranguet Vaillant J., Mallok A., Viebanh Hänsler R., Menéndez Cepero S, et al. Ozone Oxidative Postconditioning Protects Against the Injury Associated with Alcohol Withdrawal Syndrome in Rats. Ozone: Science & Engineering. 2012, 34: 425–431. https://doi.org/10.1080/01919512.2012.71 8949.