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Centro de Investigaciones Regionales Dr. Hideyo Noguchi, Universidad Autónoma de Yucatán

2020, Number 2

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Rev Biomed 2020; 31 (2)

Alcohol withdrawal syndrome: Result of oxidative stress and neuronal imbalance. State of the art

Díaz-Soto MT, Calderín-Miranda JM

Language: Spanish
References: 100
Page: 95-107
PDF size: 437.38 Kb.


ABSTRACT

Alcoholism 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.


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