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Apoptosis and Necrosis: Two Types of Cell Death in Alcoholic Liver Disease

Heavy alcohol consumption over long periods of time can result in severe liver damage, including death of liver cells (i.e., hepatocytes). Two mechanisms—apoptosis and necrosis—can contribute to hepatocyte death. In apoptosis, the affected cell actively participates in the cell death process, wherea...

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Detalles Bibliográficos
Autores principales: Nanji, Amin A., Hiller-Sturmhöfel, Susanne
Formato: Online Artículo Texto
Lenguaje:English
Publicado: National Institute on Alcohol Abuse and Alcoholism 1997
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6827678/
https://www.ncbi.nlm.nih.gov/pubmed/15706744
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author Nanji, Amin A.
Hiller-Sturmhöfel, Susanne
author_facet Nanji, Amin A.
Hiller-Sturmhöfel, Susanne
author_sort Nanji, Amin A.
collection PubMed
description Heavy alcohol consumption over long periods of time can result in severe liver damage, including death of liver cells (i.e., hepatocytes). Two mechanisms—apoptosis and necrosis—can contribute to hepatocyte death. In apoptosis, the affected cell actively participates in the cell death process, whereas in necrosis the cell death occurs in response to adverse conditions in the cell’s environment. Numerous factors that may contribute to the initiation of hepatocyte apoptosis are affected by alcohol consumption. These factors include the enzyme cytochrome P450 2E1 (i.e., CYP2E1), small molecules (i.e., cytokines) involved in cell communication, oxidative stress, and changes in iron metabolism. Similarly, alcohol consumption can influence several factors believed to be involved in hepatocyte necrosis, including depletion of the energy-storing molecule adenosine-triphosphate, reduced oxygen levels (i.e., hypoxia) in the liver, oxidative stress, and bacterial molecules called endotoxins.
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spelling pubmed-68276782019-11-07 Apoptosis and Necrosis: Two Types of Cell Death in Alcoholic Liver Disease Nanji, Amin A. Hiller-Sturmhöfel, Susanne Alcohol Health Res World Research Update Heavy alcohol consumption over long periods of time can result in severe liver damage, including death of liver cells (i.e., hepatocytes). Two mechanisms—apoptosis and necrosis—can contribute to hepatocyte death. In apoptosis, the affected cell actively participates in the cell death process, whereas in necrosis the cell death occurs in response to adverse conditions in the cell’s environment. Numerous factors that may contribute to the initiation of hepatocyte apoptosis are affected by alcohol consumption. These factors include the enzyme cytochrome P450 2E1 (i.e., CYP2E1), small molecules (i.e., cytokines) involved in cell communication, oxidative stress, and changes in iron metabolism. Similarly, alcohol consumption can influence several factors believed to be involved in hepatocyte necrosis, including depletion of the energy-storing molecule adenosine-triphosphate, reduced oxygen levels (i.e., hypoxia) in the liver, oxidative stress, and bacterial molecules called endotoxins. National Institute on Alcohol Abuse and Alcoholism 1997 /pmc/articles/PMC6827678/ /pubmed/15706744 Text en http://creativecommons.org/publicdomain/mark/1.0/ Unless otherwise noted in the text, all material appearing in this journal is in the public domain and may be reproduced without permission. Citation of the source is appreciated.
spellingShingle Research Update
Nanji, Amin A.
Hiller-Sturmhöfel, Susanne
Apoptosis and Necrosis: Two Types of Cell Death in Alcoholic Liver Disease
title Apoptosis and Necrosis: Two Types of Cell Death in Alcoholic Liver Disease
title_full Apoptosis and Necrosis: Two Types of Cell Death in Alcoholic Liver Disease
title_fullStr Apoptosis and Necrosis: Two Types of Cell Death in Alcoholic Liver Disease
title_full_unstemmed Apoptosis and Necrosis: Two Types of Cell Death in Alcoholic Liver Disease
title_short Apoptosis and Necrosis: Two Types of Cell Death in Alcoholic Liver Disease
title_sort apoptosis and necrosis: two types of cell death in alcoholic liver disease
topic Research Update
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6827678/
https://www.ncbi.nlm.nih.gov/pubmed/15706744
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