Ethanol Intake and Toxicity: In Search of New Treatments

Prolonged alcohol consumption has consequences on the liver, producing necrotic precipitates and fibrosis, on the pancreas, causing the pancreatic acini to atrophy and destroying insulin-producing cells, and on the central nervous system (CNS), causing the gray and white matter in the frontal lobes...

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Autores principales:	Sandoval,Cristian, Vásquez,Bélgica, Mandarim-de-Lacerda,Carlos, del Sol,Mariano
Lenguaje:	English
Publicado:	Sociedad Chilena de Anatomía 2017
Materias:	Antioxidants Ethanol Liver Pancreas Central nervous system
Acceso en línea:	http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0717-95022017000300024
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spelling	oai:scielo:S0717-950220170003000242017-11-20Ethanol Intake and Toxicity: In Search of New TreatmentsSandoval,CristianVásquez,BélgicaMandarim-de-Lacerda,Carlosdel Sol,Mariano Antioxidants Ethanol Liver Pancreas Central nervous system Prolonged alcohol consumption has consequences on the liver, producing necrotic precipitates and fibrosis, on the pancreas, causing the pancreatic acini to atrophy and destroying insulin-producing cells, and on the central nervous system (CNS), causing the gray and white matter in the frontal lobes of the brain and cerebellum to atrophy. Generally, alcohol is metabolized via oxidative pathways, where the enzymes alcohol dehydrogenase and aldehyde dehydrogenase participate during its metabolization in the liver and CNS, or via non-oxidative pathways during its metabolization in the pancreas. Ethanol metabolism can produce oxidative stress and tissue damage mediated by free radicals, causing morphological and functional alterations in the liver. In the pancreas, it can cause progressive and irreversible damage affecting the endocrine and exocrine functions, a result of the activation of the stellate cells, which are activated directly by alcohol, causing pancreatic fibrosis. In the CNS ethanol can bind directly to proteins, nucleic acids and phospholipids to develop its pathogenesis. The effects produced by alcohol can be counteracted by supplementation with antioxidants, which reduce the inflammation and areas of focal necrosis in the liver, inhibit the activation of pancreatic stellate cells, and reduce oxidative stress in the CNS. Additionally, in order to reduce the negative effects associated with alcohol consumption, recent studies have suggested the administration of antioxidants as a treatment strategy.info:eu-repo/semantics/openAccessSociedad Chilena de AnatomíaInternational Journal of Morphology v.35 n.3 20172017-09-01text/htmlhttp://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0717-95022017000300024en10.4067/S0717-95022017000300024
institution	Scielo Chile
collection	Scielo Chile
language	English
topic	Antioxidants Ethanol Liver Pancreas Central nervous system
spellingShingle	Antioxidants Ethanol Liver Pancreas Central nervous system Sandoval,Cristian Vásquez,Bélgica Mandarim-de-Lacerda,Carlos del Sol,Mariano Ethanol Intake and Toxicity: In Search of New Treatments
description	Prolonged alcohol consumption has consequences on the liver, producing necrotic precipitates and fibrosis, on the pancreas, causing the pancreatic acini to atrophy and destroying insulin-producing cells, and on the central nervous system (CNS), causing the gray and white matter in the frontal lobes of the brain and cerebellum to atrophy. Generally, alcohol is metabolized via oxidative pathways, where the enzymes alcohol dehydrogenase and aldehyde dehydrogenase participate during its metabolization in the liver and CNS, or via non-oxidative pathways during its metabolization in the pancreas. Ethanol metabolism can produce oxidative stress and tissue damage mediated by free radicals, causing morphological and functional alterations in the liver. In the pancreas, it can cause progressive and irreversible damage affecting the endocrine and exocrine functions, a result of the activation of the stellate cells, which are activated directly by alcohol, causing pancreatic fibrosis. In the CNS ethanol can bind directly to proteins, nucleic acids and phospholipids to develop its pathogenesis. The effects produced by alcohol can be counteracted by supplementation with antioxidants, which reduce the inflammation and areas of focal necrosis in the liver, inhibit the activation of pancreatic stellate cells, and reduce oxidative stress in the CNS. Additionally, in order to reduce the negative effects associated with alcohol consumption, recent studies have suggested the administration of antioxidants as a treatment strategy.
author	Sandoval,Cristian Vásquez,Bélgica Mandarim-de-Lacerda,Carlos del Sol,Mariano
author_facet	Sandoval,Cristian Vásquez,Bélgica Mandarim-de-Lacerda,Carlos del Sol,Mariano
author_sort	Sandoval,Cristian
title	Ethanol Intake and Toxicity: In Search of New Treatments
title_short	Ethanol Intake and Toxicity: In Search of New Treatments
title_full	Ethanol Intake and Toxicity: In Search of New Treatments
title_fullStr	Ethanol Intake and Toxicity: In Search of New Treatments
title_full_unstemmed	Ethanol Intake and Toxicity: In Search of New Treatments
title_sort	ethanol intake and toxicity: in search of new treatments
publisher	Sociedad Chilena de Anatomía
publishDate	2017
url	http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0717-95022017000300024
work_keys_str_mv	AT sandovalcristian ethanolintakeandtoxicityinsearchofnewtreatments AT vasquezbelgica ethanolintakeandtoxicityinsearchofnewtreatments AT mandarimdelacerdacarlos ethanolintakeandtoxicityinsearchofnewtreatments AT delsolmariano ethanolintakeandtoxicityinsearchofnewtreatments
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Ethanol Intake and Toxicity: In Search of New Treatments

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