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Revista Med

versão impressa ISSN 0121-5256

Resumo

SCHLESINGER PIEDRAHITA, ANTONIO; PESCADOR VARGAS, BEATRIZ  e  ROA CULMA, LAURA ALEJANDRA. ALCOHOLIC NEUROTOXICITY. rev.fac.med [online]. 2017, vol.25, n.1, pp.87-101. ISSN 0121-5256.  https://doi.org/10.18359/rmed.2924.

Alcohol is a toxic that acts as a central nervous system (CNS) depressant. Its effects are a direct consequence of its action on cell membranes and on neurotransmitters. Neurons are particularly sensitive to the neurotoxic effect of Ethanol (EtOH) and their exposure affects neuronal morphology, since a reduction in the length of the dendritic tree has recently been observed. EtOH also causes changes in the expression of synaptic proteins, increased endoplasmic reticulum light, as well as disorganization of the Golgi apparatus and mitochondria. Objectives: To describe the effects of Ethanol at the cellular and molecular level in the Central Nervous System and its repercussion on human health. Methods: A literature search was conducted in the following databases available on the web: PubMed, ScienceDirect, Jama Journal, Scielo and health portals, using the keywords: "ethanol and pharmacology", "alcohol and toxicology", "Neurotoxicity and ethanol". Results: From the databases consulted, a total of 120 references were obtained, of which 55 are accepted, highlighting the most relevant pathophysiology of ethanol intoxication and the minimum number of molecular levels related to the effects on the CNS. Conclusions: The effects of EtOH on the nervous system can be a consequence of an acute and excessive consumption or secondary to a chronic consumption, in relation to a state of addiction and dependence to it. The toxicity on the nervous system is the direct consequence of the aggression of ethanol and the different metabolic disorders linked to the toxicity of the same on other organs. The neurotoxicity of alcohol is due to the activation of the immune system in the brain, which promotes inflammatory cascade that cause those responsible for neuron damage, in addition to neuroanalytic alteration of the cortex.

Palavras-chave : Alcoholism; Neurotoxicity; Synapse; Cell death; Apoptosis.

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