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<a href="http://doi.org/10.1016/bs.apha.2015.04.002" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/bs.apha.2015.04.002</a>
Pages
303–372
Volume
74
Dublin Core
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Title
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Translational Implications of the Alcohol-Metabolizing Enzymes, Including Cytochrome P450-2E1, in Alcoholic and Nonalcoholic Liver Disease.
Publisher
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Advances in pharmacology (San Diego, Calif.)
Date
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2015
2015
Subject
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Alcohol-metabolizing enzymes; Alcoholic/*enzymology/*metabolism; ALDH2; Animals; CYP2E1; Cytochrome P-450 CYP2E1/*metabolism; Ethanol/*metabolism; Humans; Liver disease; Liver Diseases; Mitochondrial dysfunction; Nitroxidative stress; Non-alcoholic Fatty Liver Disease/*enzymology/*metabolism; Posttranslational modifications
Creator
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Song Byoung-Joon; Akbar Mohammed; Jo Inho; Hardwick James P; Abdelmegeed Mohamed A
Description
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Fat accumulation (hepatic steatosis) in alcoholic and nonalcoholic fatty liver disease is a potentially pathologic condition which can progress to steatohepatitis (inflammation), fibrosis, cirrhosis, and carcinogenesis. Many clinically used drugs or some alternative medicine compounds are also known to cause drug-induced liver injury, which can further lead to fulminant liver failure and acute deaths in extreme cases. During liver disease process, certain cytochromes P450 such as the ethanol-inducible cytochrome P450-2E1 (CYP2E1) and CYP4A isozymes can be induced and/or activated by alcohol and/or high-fat diets and pathophysiological conditions such as fasting, obesity, and diabetes. Activation of these P450 isozymes, involved in the metabolism of ethanol, fatty acids, and various drugs, can produce reactive oxygen/nitrogen species directly and/or indirectly, contributing to oxidative modifications of DNA/RNA, proteins and lipids. In addition, aldehyde dehydrogenases including the mitochondrial low Km aldehyde dehydrogenase-2 (ALDH2), responsible for the metabolism of acetaldehyde and lipid aldehydes, can be inactivated by various hepatotoxic agents. These highly reactive acetaldehyde and lipid peroxides, accumulated due to ALDH2 suppression, can interact with cellular macromolecules DNA/RNA, lipids, and proteins, leading to suppression of their normal function, contributing to DNA mutations, endoplasmic reticulum stress, mitochondrial dysfunction, steatosis, and cell death. In this chapter, we specifically review the roles of the alcohol-metabolizing enzymes including the alcohol dehydrogenase, ALDH2, CYP2E1, and other enzymes in promoting liver disease. We also discuss translational research opportunities with natural and/or synthetic antioxidants, which can prevent or delay the onset of inflammation and liver disease.
Identifier
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<a href="http://doi.org/10.1016/bs.apha.2015.04.002" target="_blank" rel="noreferrer noopener">10.1016/bs.apha.2015.04.002</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2015
Abdelmegeed Mohamed A
Advances in pharmacology (San Diego, Calif.)
Akbar Mohammed
Alcohol-metabolizing enzymes
Alcoholic/*enzymology/*metabolism
ALDH2
Animals
CYP2E1
Cytochrome P-450 CYP2E1/*metabolism
Department of Integrative Medical Sciences
Ethanol/*metabolism
Hardwick James P
Humans
Jo Inho
Liver disease
Liver Diseases
Mitochondrial dysfunction
NEOMED College of Medicine
Nitroxidative stress
Non-alcoholic Fatty Liver Disease/*enzymology/*metabolism
Posttranslational modifications
Song Byoung-Joon