Redox regulation of hepatitis C in nonalcoholic and alcoholic liver
Hepatitis C virus (HCV) is an RNA virus of the Flaviviridae family that is estimated to have infected 170 million people worldwide. HCV can cause serious liver disease in humans, such as cirrhosis, steatosis, and hepatocellular carcinoma. HCV induces a state of oxidative/nitrosative stress in patien...
Gespeichert in:
| Veröffentlicht in: | Free radical biology & medicine 2007-09, Vol.43 (6), p.869-882 |
|---|---|
| Hauptverfasser: | , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 882 |
|---|---|
| container_issue | 6 |
| container_start_page | 869 |
| container_title | Free radical biology & medicine |
| container_volume | 43 |
| creator | Seronello, Scott Sheikh, Muhammad Y. Choi, Jinah |
| description | Hepatitis C virus (HCV) is an RNA virus of the
Flaviviridae family that is estimated to have infected 170 million people worldwide. HCV can cause serious liver disease in humans, such as cirrhosis, steatosis, and hepatocellular carcinoma. HCV induces a state of oxidative/nitrosative stress in patients through multiple mechanisms, and this redox perturbation has been recognized as a key player in HCV-induced pathogenesis. Studies have shown that alcohol synergizes with HCV in the pathogenesis of liver disease, and part of these effects may be mediated by reactive species that are generated during hepatic metabolism of alcohol. Furthermore, reactive species and alcohol may influence HCV replication and the outcome of interferon therapy. Alcohol consumption has also been associated with increased sequence heterogeneity of the HCV RNA sequences, suggesting multiple modes of interaction between alcohol and HCV. This review summarizes the current understanding of oxidative and nitrosative stress during HCV infection and possible combined effects of HCV, alcohol, and reactive species in the pathogenesis of liver disease. |
| doi_str_mv | 10.1016/j.freeradbiomed.2007.05.036 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_20642187</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0891584907003942</els_id><sourcerecordid>20642187</sourcerecordid><originalsourceid>FETCH-LOGICAL-c531t-dae90b5d2857ad82c448ac3658631304e8f4901df6603dfbab82f163e002b5893</originalsourceid><addsrcrecordid>eNqNkN9LwzAQx4Mobk7_BSkIvrVemiZN8UnG_AEDQfQ5pMnVZXTNTLqh_70dG4pvPt0d97378v0QckUho0DFzTJrAmLQtnZ-hTbLAcoMeAZMHJExlSVLC16JYzIGWdGUy6IakbMYlwBQcCZPyYiWoiorlo_J9AWt_0wCvm9a3TvfJb5JFrge-t7FZJq4Lul8p1vjF751JtGdTX6n1m0xnJOTRrcRLw51Qt7uZ6_Tx3T-_PA0vZunhjPap1ZjBTW3ueSltjI3RSG1YYJLwSiDAmVTVEBtIwQw29S6lnlDBUOAvOayYhNyvf-7Dv5jg7FXKxcNtq3u0G-iykEU-S7_hNzuhSb4GAM2ah3cSocvRUHtGKql-sNQ7Rgq4GpgOFxfHmw29W73c3uANghmewEOYbcOg4rGYWfQuoCmV9a7fxl9A-HNihU</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>20642187</pqid></control><display><type>article</type><title>Redox regulation of hepatitis C in nonalcoholic and alcoholic liver</title><source>MEDLINE</source><source>Elsevier ScienceDirect Journals</source><creator>Seronello, Scott ; Sheikh, Muhammad Y. ; Choi, Jinah</creator><creatorcontrib>Seronello, Scott ; Sheikh, Muhammad Y. ; Choi, Jinah</creatorcontrib><description>Hepatitis C virus (HCV) is an RNA virus of the
Flaviviridae family that is estimated to have infected 170 million people worldwide. HCV can cause serious liver disease in humans, such as cirrhosis, steatosis, and hepatocellular carcinoma. HCV induces a state of oxidative/nitrosative stress in patients through multiple mechanisms, and this redox perturbation has been recognized as a key player in HCV-induced pathogenesis. Studies have shown that alcohol synergizes with HCV in the pathogenesis of liver disease, and part of these effects may be mediated by reactive species that are generated during hepatic metabolism of alcohol. Furthermore, reactive species and alcohol may influence HCV replication and the outcome of interferon therapy. Alcohol consumption has also been associated with increased sequence heterogeneity of the HCV RNA sequences, suggesting multiple modes of interaction between alcohol and HCV. This review summarizes the current understanding of oxidative and nitrosative stress during HCV infection and possible combined effects of HCV, alcohol, and reactive species in the pathogenesis of liver disease.</description><identifier>ISSN: 0891-5849</identifier><identifier>EISSN: 1873-4596</identifier><identifier>DOI: 10.1016/j.freeradbiomed.2007.05.036</identifier><identifier>PMID: 17697932</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Acetaldehyde ; Alcohol ; Antioxidant ; Chemical and Drug Induced Liver Injury ; Ethanol - toxicity ; Evolution ; Flaviviridae ; Free radicals ; Hepacivirus - pathogenicity ; Hepatitis C - complications ; Hepatitis C - metabolism ; Hepatitis C virus ; Hepatocellular carcinoma ; Humans ; Liver Diseases - metabolism ; Liver Diseases - virology ; Liver Diseases, Alcoholic - metabolism ; Liver Diseases, Alcoholic - virology ; Nitrosative stress ; Oxidation-Reduction ; Oxidative Stress ; Pathogenesis ; Reactive Oxygen Species - toxicity ; Replication</subject><ispartof>Free radical biology & medicine, 2007-09, Vol.43 (6), p.869-882</ispartof><rights>2007 Elsevier Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c531t-dae90b5d2857ad82c448ac3658631304e8f4901df6603dfbab82f163e002b5893</citedby><cites>FETCH-LOGICAL-c531t-dae90b5d2857ad82c448ac3658631304e8f4901df6603dfbab82f163e002b5893</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0891584907003942$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27903,27904,65309</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17697932$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Seronello, Scott</creatorcontrib><creatorcontrib>Sheikh, Muhammad Y.</creatorcontrib><creatorcontrib>Choi, Jinah</creatorcontrib><title>Redox regulation of hepatitis C in nonalcoholic and alcoholic liver</title><title>Free radical biology & medicine</title><addtitle>Free Radic Biol Med</addtitle><description>Hepatitis C virus (HCV) is an RNA virus of the
Flaviviridae family that is estimated to have infected 170 million people worldwide. HCV can cause serious liver disease in humans, such as cirrhosis, steatosis, and hepatocellular carcinoma. HCV induces a state of oxidative/nitrosative stress in patients through multiple mechanisms, and this redox perturbation has been recognized as a key player in HCV-induced pathogenesis. Studies have shown that alcohol synergizes with HCV in the pathogenesis of liver disease, and part of these effects may be mediated by reactive species that are generated during hepatic metabolism of alcohol. Furthermore, reactive species and alcohol may influence HCV replication and the outcome of interferon therapy. Alcohol consumption has also been associated with increased sequence heterogeneity of the HCV RNA sequences, suggesting multiple modes of interaction between alcohol and HCV. This review summarizes the current understanding of oxidative and nitrosative stress during HCV infection and possible combined effects of HCV, alcohol, and reactive species in the pathogenesis of liver disease.</description><subject>Acetaldehyde</subject><subject>Alcohol</subject><subject>Antioxidant</subject><subject>Chemical and Drug Induced Liver Injury</subject><subject>Ethanol - toxicity</subject><subject>Evolution</subject><subject>Flaviviridae</subject><subject>Free radicals</subject><subject>Hepacivirus - pathogenicity</subject><subject>Hepatitis C - complications</subject><subject>Hepatitis C - metabolism</subject><subject>Hepatitis C virus</subject><subject>Hepatocellular carcinoma</subject><subject>Humans</subject><subject>Liver Diseases - metabolism</subject><subject>Liver Diseases - virology</subject><subject>Liver Diseases, Alcoholic - metabolism</subject><subject>Liver Diseases, Alcoholic - virology</subject><subject>Nitrosative stress</subject><subject>Oxidation-Reduction</subject><subject>Oxidative Stress</subject><subject>Pathogenesis</subject><subject>Reactive Oxygen Species - toxicity</subject><subject>Replication</subject><issn>0891-5849</issn><issn>1873-4596</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkN9LwzAQx4Mobk7_BSkIvrVemiZN8UnG_AEDQfQ5pMnVZXTNTLqh_70dG4pvPt0d97378v0QckUho0DFzTJrAmLQtnZ-hTbLAcoMeAZMHJExlSVLC16JYzIGWdGUy6IakbMYlwBQcCZPyYiWoiorlo_J9AWt_0wCvm9a3TvfJb5JFrge-t7FZJq4Lul8p1vjF751JtGdTX6n1m0xnJOTRrcRLw51Qt7uZ6_Tx3T-_PA0vZunhjPap1ZjBTW3ueSltjI3RSG1YYJLwSiDAmVTVEBtIwQw29S6lnlDBUOAvOayYhNyvf-7Dv5jg7FXKxcNtq3u0G-iykEU-S7_hNzuhSb4GAM2ah3cSocvRUHtGKql-sNQ7Rgq4GpgOFxfHmw29W73c3uANghmewEOYbcOg4rGYWfQuoCmV9a7fxl9A-HNihU</recordid><startdate>20070915</startdate><enddate>20070915</enddate><creator>Seronello, Scott</creator><creator>Sheikh, Muhammad Y.</creator><creator>Choi, Jinah</creator><general>Elsevier Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7U7</scope><scope>7U9</scope><scope>C1K</scope><scope>H94</scope></search><sort><creationdate>20070915</creationdate><title>Redox regulation of hepatitis C in nonalcoholic and alcoholic liver</title><author>Seronello, Scott ; Sheikh, Muhammad Y. ; Choi, Jinah</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c531t-dae90b5d2857ad82c448ac3658631304e8f4901df6603dfbab82f163e002b5893</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Acetaldehyde</topic><topic>Alcohol</topic><topic>Antioxidant</topic><topic>Chemical and Drug Induced Liver Injury</topic><topic>Ethanol - toxicity</topic><topic>Evolution</topic><topic>Flaviviridae</topic><topic>Free radicals</topic><topic>Hepacivirus - pathogenicity</topic><topic>Hepatitis C - complications</topic><topic>Hepatitis C - metabolism</topic><topic>Hepatitis C virus</topic><topic>Hepatocellular carcinoma</topic><topic>Humans</topic><topic>Liver Diseases - metabolism</topic><topic>Liver Diseases - virology</topic><topic>Liver Diseases, Alcoholic - metabolism</topic><topic>Liver Diseases, Alcoholic - virology</topic><topic>Nitrosative stress</topic><topic>Oxidation-Reduction</topic><topic>Oxidative Stress</topic><topic>Pathogenesis</topic><topic>Reactive Oxygen Species - toxicity</topic><topic>Replication</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Seronello, Scott</creatorcontrib><creatorcontrib>Sheikh, Muhammad Y.</creatorcontrib><creatorcontrib>Choi, Jinah</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>AIDS and Cancer Research Abstracts</collection><jtitle>Free radical biology & medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Seronello, Scott</au><au>Sheikh, Muhammad Y.</au><au>Choi, Jinah</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Redox regulation of hepatitis C in nonalcoholic and alcoholic liver</atitle><jtitle>Free radical biology & medicine</jtitle><addtitle>Free Radic Biol Med</addtitle><date>2007-09-15</date><risdate>2007</risdate><volume>43</volume><issue>6</issue><spage>869</spage><epage>882</epage><pages>869-882</pages><issn>0891-5849</issn><eissn>1873-4596</eissn><abstract>Hepatitis C virus (HCV) is an RNA virus of the
Flaviviridae family that is estimated to have infected 170 million people worldwide. HCV can cause serious liver disease in humans, such as cirrhosis, steatosis, and hepatocellular carcinoma. HCV induces a state of oxidative/nitrosative stress in patients through multiple mechanisms, and this redox perturbation has been recognized as a key player in HCV-induced pathogenesis. Studies have shown that alcohol synergizes with HCV in the pathogenesis of liver disease, and part of these effects may be mediated by reactive species that are generated during hepatic metabolism of alcohol. Furthermore, reactive species and alcohol may influence HCV replication and the outcome of interferon therapy. Alcohol consumption has also been associated with increased sequence heterogeneity of the HCV RNA sequences, suggesting multiple modes of interaction between alcohol and HCV. This review summarizes the current understanding of oxidative and nitrosative stress during HCV infection and possible combined effects of HCV, alcohol, and reactive species in the pathogenesis of liver disease.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>17697932</pmid><doi>10.1016/j.freeradbiomed.2007.05.036</doi><tpages>14</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0891-5849 |
| ispartof | Free radical biology & medicine, 2007-09, Vol.43 (6), p.869-882 |
| issn | 0891-5849 1873-4596 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_20642187 |
| source | MEDLINE; Elsevier ScienceDirect Journals |
| subjects | Acetaldehyde Alcohol Antioxidant Chemical and Drug Induced Liver Injury Ethanol - toxicity Evolution Flaviviridae Free radicals Hepacivirus - pathogenicity Hepatitis C - complications Hepatitis C - metabolism Hepatitis C virus Hepatocellular carcinoma Humans Liver Diseases - metabolism Liver Diseases - virology Liver Diseases, Alcoholic - metabolism Liver Diseases, Alcoholic - virology Nitrosative stress Oxidation-Reduction Oxidative Stress Pathogenesis Reactive Oxygen Species - toxicity Replication |
| title | Redox regulation of hepatitis C in nonalcoholic and alcoholic liver |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-27T11%3A02%3A19IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Redox%20regulation%20of%20hepatitis%20C%20in%20nonalcoholic%20and%20alcoholic%20liver&rft.jtitle=Free%20radical%20biology%20&%20medicine&rft.au=Seronello,%20Scott&rft.date=2007-09-15&rft.volume=43&rft.issue=6&rft.spage=869&rft.epage=882&rft.pages=869-882&rft.issn=0891-5849&rft.eissn=1873-4596&rft_id=info:doi/10.1016/j.freeradbiomed.2007.05.036&rft_dat=%3Cproquest_cross%3E20642187%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=20642187&rft_id=info:pmid/17697932&rft_els_id=S0891584907003942&rfr_iscdi=true |