Contributing Roles of CYP2E1 and Other Cytochrome P450 Isoforms in Alcohol-Related Tissue Injury and Carcinogenesis

Song, Byoung–Joon; Abdelmegeed, Mohamed A.; Cho, Young-Eun; Akbar, Mohammed; Rhim, Johng S.; Song, Minkyung; Hardwick, James P.

doi:10.1007/978-3-030-22254-3_6

Cited by 26 publications

(18 citation statements)

References 142 publications

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“…In contrast to those of ADH and catalase, CYP2E1 expression and activity are usually induced by ethanol and other substances, such as dietary fats. The induction and activation of CYP2E1, in turn, contribute to alcohol-and nonalcohol-induced pathophysiology [136][137][138][139][140][141][142][143][144] . In the second step, acetaldehyde is converted to acetate due to the low km (for acetaldehyde) mitochondrial aldehyde dehydrogenase 2 isozyme (ALDH2) in humans 145 .…”

Section: Hepatic Alcohol Metabolismmentioning

confidence: 99%

Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury

et al. 2021

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Advanced glycation end products (AGEs) are potentially harmful and heterogeneous molecules derived from nonenzymatic glycation. The pathological implications of AGEs are ascribed to their ability to promote oxidative stress, inflammation, and apoptosis. Recent studies in basic and translational research have revealed the contributing roles of AGEs in the development and progression of various aging-related pathological conditions, such as diabetes, cardiovascular complications, gut microbiome-associated illnesses, liver or neurodegenerative diseases, and cancer. Excessive chronic and/or acute binge consumption of alcohol (ethanol), a widely consumed addictive substance, is known to cause more than 200 diseases, including alcohol use disorder (addiction), alcoholic liver disease, and brain damage. However, despite the considerable amount of research in this area, the underlying molecular mechanisms by which alcohol abuse causes cellular toxicity and organ damage remain to be further characterized. In this review, we first briefly describe the properties of AGEs: their formation, accumulation, and receptor interactions. We then focus on the causative functions of AGEs that impact various aging-related diseases. We also highlight the biological connection of AGE–alcohol–adduct formations to alcohol-mediated tissue injury. Finally, we describe the potential translational research opportunities for treatment of various AGE- and/or alcohol-related adduct-associated disorders according to the mechanistic insights presented.

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Section: Hepatic Alcohol Metabolismmentioning

confidence: 99%

Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury

et al. 2021

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“…Cytochrome P450 family 2 subfamily E member 1 ( CYP2E1 ) was found to be the gene with significant difference between the two microarrays. Human cytochrome P450 (CYP) is a phase I enzyme which plays an important role in the metabolic activation of numerous procarcinogens ( 26 ). CYP2E1 represents a major CYP isoform.…”

Section: Discussionmentioning

confidence: 99%

Identification of potential biomarkers and available drugs for oral squamous cell carcinoma

Zhang¹,

Bi²,

Zhang³

et al. 2021

Transl Cancer Res TCR

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Background: Oral squamous cell carcinoma (OSCC) is the most common oral tumor globally. However, optimal therapeutic targets for OSCC have not been identified. This study aimed to identify the potential gene markers and available drugs for OSCC.Methods: Two transcriptional datasets containing OSCC gene expression data (GSE30784 and GSE23558) were selected from the Gene Expression Omnibus database. The interactive web tool GEO2R was then used to analyze the differentially expressed genes (DEGs) analysis. A Venn diagram was used to integrate the DEGs screened out by the two microarrays. Subsequently, a protein-protein interaction (PPI) network analysis of DEGs was performed using the Cytoscape, Database for Annotation, Visualization and Intergrated Discovery, and STRING databases. In addition to constructing the PPI networks among these DEGs, we chose several significant gene modules to conduct further gene-drug interaction analyses. Lastly, the existing drugs that target these module genes were selected to explore their therapeutic efficacy in treating OSCC.Results: A total of 199 DEGs were screened out by the two microarrays. They were found to be associated with several processes, including the epoxygenase P450 pathway and the organelle membrane. The significant module genes in the PPI networks were CYP2E1, SCEL, KRT4, and KRT19. One existing drug, etoposide, which targets the CYP2E1 gene, was acquired.Conclusions: Four potential biomarkers (CYP2E1, SCEL, KRT4, and KRT19) and one existing drug (etoposide) were obtained for gene expression prediction through a series of bioinformatics methods.

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“…The pathogenesis of alcohol fatty liver is complex, but the essence is mainly through the influence of alcohol dehydrogenase (ADH) (70–80%) and cytochrome P4502E1 (CYP2E1) enzyme activity [ 78 ] of microsomal ethanol oxidation system (MEOS) (10–25%), influence of ethanol metabolism; ADH enzyme activity [ 79 ] regulates lipid metabolism by affecting SIRT1 [ 80 ], AMPK [ 79 ], SREBP-1C, ChREBP, and PPAR- α . Moreover, CYP2E1 can induce oxidative stress, autophagy, and apoptosis via producing a series of ROS and endotoxin after alcohol [ 4 ]; the study shows PCP in the treatment of alcohol fatty liver from the essence of the ADH, CYP2E1 enzyme activity, and then it regulates ethanol metabolism, which is unified with the theory of Chinese medicine “both the symptoms and the treatment.”…”

Section: Discussionmentioning

confidence: 99%

An Overview of the Mechanism of Penthorum chinense Pursh on Alcoholic Fatty Liver

Zhao

Liao

Zhou

et al. 2020

Evidence-Based Complementary and Alternative Medicine

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Alcohol liver disease (ALD) caused by excessive alcohol consumption is a progressive disease, and alcohol fatty liver disease is the primary stage. Currently, there is no approved drug for its treatment. Abstinence is the best way to heal, but patients’ compliance is poor. Unlike other chronic diseases, alcohol fatty liver disease is not caused by nutritional deficiencies; it is caused by the molecular action of ingested alcohol and its metabolites. More and more studies have shown the potential of Penthorum chinense Pursh (PCP) in the clinical use of alcohol fatty liver treatment. The purpose of this paper is to reveal from the essence of PCP treatment of alcohol liver mechanism mainly by the ethanol dehydrogenase (ADH) and microsomal ethanol oxidation system-dependent cytochrome P4502E1 (CYP2E1) to exert antilipogenesis, antioxidant, anti-inflammatory, antiapoptotic, and autophagy effects, with special emphasis on its mechanisms related to SIRT1/AMPK, KEAP-1/Nrf2, and TLR4/NF-κB. Overall, data from the literature shows that PCP appears to be a promising hepatoprotective traditional Chinese medicine (TCM).

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Contributing Roles of CYP2E1 and Other Cytochrome P450 Isoforms in Alcohol-Related Tissue Injury and Carcinogenesis

Cited by 26 publications

References 142 publications

Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury

Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury

Identification of potential biomarkers and available drugs for oral squamous cell carcinoma

An Overview of the Mechanism of Penthorum chinense Pursh on Alcoholic Fatty Liver

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