| Literature DB >> 29637855 |
Yongke Lu1,2, Arthur I Cederbaum3.
Abstract
Alcohol consumption causes liver diseases, designated as Alcoholic Liver Disease (ALD). Because alcohol is detoxified by alcohol dehydrogenase (ADH), a major ethanol metabolism system, the development of ALD was initially believed to be due to malnutrition caused by alcohol metabolism in liver. The discovery of the microsomal ethanol oxidizing system (MEOS) changed this dogma. Cytochrome P450 enzymes (CYP) constitute the major components of MEOS. Cytochrome P450 2E1 (CYP2E1) in MEOS is one of the major ROS generators in liver and is considered to be contributive to ALD. Our labs have been studying the relationship between CYP2E1 and ALD for many years. Recently, we found that human CYP2A6 and its mouse analog CYP2A5 are also induced by alcohol. In mice, the alcohol induction of CYP2A5 is CYP2E1-dependent. Unlike CYP2E1, CYP2A5 protects against the development of ALD. The relationship of CYP2E1, CYP2A5, and ALD is a major focus of this review. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.org.Entities:
Keywords: Alcohol induction; CYP2A5; CYP2A6; CYP2E1; FGF21; HIF-1α; LPS; MAPK; Nrf2; PPARα; TNFα; alcoholiczzm321990liver disease; antioxidants; autophagy; coumarin 7-hydroxylase; interactions; liver fibrosis; nicotine; pyrazole; reactive oxygen species.
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Year: 2018 PMID： 29637855 PMCID： PMC6053342 DOI： 10.2174/1381612824666180410091511
Source DB: PubMed Journal: Curr Pharm Des ISSN： 1381-6128 Impact factor: 3.116