Oxidative Stress and Pulmonary Changes in Experimental Liver Cirrhosis
The use of carbon tetrachloride (CCl4) in rats is an experimental model of hepatic tissue damage; which leads to fibrosis, and at the long term, cirrhosis. Cirrhosis is the consequence of progressive continued liver damage, it may be reversible when the damaging noxae have been withdrawn. The aim of...
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| container_title | Oxidative medicine and cellular longevity |
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| creator | Salatti Ferrari, Renata da Rosa, Darlan Pase Forgiarini, Luiz Felipe Bona, Sílvia Simões Dias, Alexandre Marroni, Norma Anair Possa |
| description | The use of carbon tetrachloride (CCl4) in rats is an experimental model of hepatic tissue damage; which leads to fibrosis, and at the long term, cirrhosis. Cirrhosis is the consequence of progressive continued liver damage, it may be reversible when the damaging noxae have been withdrawn. The aim of this study is to evaluate the changes caused by cirrhosis in lung and liver, through the experimental model of intraperitoneal CCI4 administration. We used 18 male Wistar rats divided into three groups: control (CO) and two groups divided by the time of cirrhosis induction by CCI4: G1 (11 weeks), G2 (16 weeks). We found significant increase of transaminase levels and lipid peroxidation (TBARS) in liver and lung tissue and also increased antioxidant enzymes SOD and CAT, as well as the expression of TNF-α and IL-1β in the lung of cirrhotic animals. We observed changes in gas exchange in both cirrhotic groups. We can conclude that our model reproduces a model of liver cirrhosis, which causes alterations in the pulmonary system that leads to changes in gas exchange and size of pulmonary vessels. |
| doi_str_mv | 10.1155/2012/486190 |
| format | Article |
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Cirrhosis is the consequence of progressive continued liver damage, it may be reversible when the damaging noxae have been withdrawn. The aim of this study is to evaluate the changes caused by cirrhosis in lung and liver, through the experimental model of intraperitoneal CCI4 administration. We used 18 male Wistar rats divided into three groups: control (CO) and two groups divided by the time of cirrhosis induction by CCI4: G1 (11 weeks), G2 (16 weeks). We found significant increase of transaminase levels and lipid peroxidation (TBARS) in liver and lung tissue and also increased antioxidant enzymes SOD and CAT, as well as the expression of TNF-α and IL-1β in the lung of cirrhotic animals. We observed changes in gas exchange in both cirrhotic groups. We can conclude that our model reproduces a model of liver cirrhosis, which causes alterations in the pulmonary system that leads to changes in gas exchange and size of pulmonary vessels.</description><identifier>ISSN: 1942-0900</identifier><identifier>EISSN: 1942-0994</identifier><identifier>DOI: 10.1155/2012/486190</identifier><identifier>PMID: 23316268</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Puplishing Corporation</publisher><subject>Animals ; Arteries - metabolism ; Blood Gas Analysis ; Catalase - metabolism ; Interleukin-1beta - metabolism ; Liver - enzymology ; Liver - pathology ; Liver Cirrhosis, Experimental - pathology ; Lung - enzymology ; Lung - pathology ; Male ; Oxidative Stress ; Rats ; Rats, Wistar ; Superoxide Dismutase - metabolism ; Thiobarbituric Acid Reactive Substances - metabolism ; Tumor Necrosis Factor-alpha - metabolism</subject><ispartof>Oxidative medicine and cellular longevity, 2012-01, Vol.2012 (2012), p.1-8</ispartof><rights>Copyright © 2012 Renata Salatti Ferrari et al.</rights><rights>Copyright © 2012 Renata Salatti Ferrari et al. 2012</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c438t-5b01c15061814a7cc83e440ee9d0dbba604d988a8eee0bf0f58b69e631103cfe3</citedby><cites>FETCH-LOGICAL-c438t-5b01c15061814a7cc83e440ee9d0dbba604d988a8eee0bf0f58b69e631103cfe3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3533490/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3533490/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23316268$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Tirosh, Oren</contributor><creatorcontrib>Salatti Ferrari, Renata</creatorcontrib><creatorcontrib>da Rosa, Darlan Pase</creatorcontrib><creatorcontrib>Forgiarini, Luiz Felipe</creatorcontrib><creatorcontrib>Bona, Sílvia</creatorcontrib><creatorcontrib>Simões Dias, Alexandre</creatorcontrib><creatorcontrib>Marroni, Norma Anair Possa</creatorcontrib><title>Oxidative Stress and Pulmonary Changes in Experimental Liver Cirrhosis</title><title>Oxidative medicine and cellular longevity</title><addtitle>Oxid Med Cell Longev</addtitle><description>The use of carbon tetrachloride (CCl4) in rats is an experimental model of hepatic tissue damage; which leads to fibrosis, and at the long term, cirrhosis. Cirrhosis is the consequence of progressive continued liver damage, it may be reversible when the damaging noxae have been withdrawn. The aim of this study is to evaluate the changes caused by cirrhosis in lung and liver, through the experimental model of intraperitoneal CCI4 administration. We used 18 male Wistar rats divided into three groups: control (CO) and two groups divided by the time of cirrhosis induction by CCI4: G1 (11 weeks), G2 (16 weeks). We found significant increase of transaminase levels and lipid peroxidation (TBARS) in liver and lung tissue and also increased antioxidant enzymes SOD and CAT, as well as the expression of TNF-α and IL-1β in the lung of cirrhotic animals. We observed changes in gas exchange in both cirrhotic groups. We can conclude that our model reproduces a model of liver cirrhosis, which causes alterations in the pulmonary system that leads to changes in gas exchange and size of pulmonary vessels.</description><subject>Animals</subject><subject>Arteries - metabolism</subject><subject>Blood Gas Analysis</subject><subject>Catalase - metabolism</subject><subject>Interleukin-1beta - metabolism</subject><subject>Liver - enzymology</subject><subject>Liver - pathology</subject><subject>Liver Cirrhosis, Experimental - pathology</subject><subject>Lung - enzymology</subject><subject>Lung - pathology</subject><subject>Male</subject><subject>Oxidative Stress</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Superoxide Dismutase - metabolism</subject><subject>Thiobarbituric Acid Reactive Substances - metabolism</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><issn>1942-0900</issn><issn>1942-0994</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>RHX</sourceid><sourceid>EIF</sourceid><recordid>eNqFkEFLw0AQhRdRrFZPnpU9K7Gz2c12cxEktCoUKqjnZZNMmpU0Kbttrf_elGjQk6cZmO-9eTxCLhjcMhZFoxBYOBJKshgOyAmLRRhAHIvDfgcYkFPv3wEkDwU7JoOQcyZDqU7IdL6zuVnbLdKXtUPvqalz-ryplk1t3CdNSlMv0FNb08luhc4usV6bis5ahaOJda5svPVn5Kgwlcfz7zkkb9PJa_IYzOYPT8n9LMgEV-sgSoFlLALJFBNmnGWKoxCAGOeQp6mRIPJYKaMQEdICikilMkbJGQOeFciH5K7zXW3SJeZZG8aZSq_aXG1a3Rir_15qW-pFs9U84lzE0BrcdAaZa7x3WPRaBnpfp97Xqbs6W_rq97ue_emvBa47oLR1bj7sP26XHYwtgoXpYTGOhGT8C87Lh-U</recordid><startdate>20120101</startdate><enddate>20120101</enddate><creator>Salatti Ferrari, Renata</creator><creator>da Rosa, Darlan Pase</creator><creator>Forgiarini, Luiz Felipe</creator><creator>Bona, Sílvia</creator><creator>Simões Dias, Alexandre</creator><creator>Marroni, Norma Anair Possa</creator><general>Hindawi Puplishing Corporation</general><general>Hindawi Publishing Corporation</general><scope>ADJCN</scope><scope>AHFXO</scope><scope>RHU</scope><scope>RHW</scope><scope>RHX</scope><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>5PM</scope></search><sort><creationdate>20120101</creationdate><title>Oxidative Stress and Pulmonary Changes in Experimental Liver Cirrhosis</title><author>Salatti Ferrari, Renata ; da Rosa, Darlan Pase ; Forgiarini, Luiz Felipe ; Bona, Sílvia ; Simões Dias, Alexandre ; Marroni, Norma Anair Possa</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c438t-5b01c15061814a7cc83e440ee9d0dbba604d988a8eee0bf0f58b69e631103cfe3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Animals</topic><topic>Arteries - metabolism</topic><topic>Blood Gas Analysis</topic><topic>Catalase - metabolism</topic><topic>Interleukin-1beta - metabolism</topic><topic>Liver - enzymology</topic><topic>Liver - pathology</topic><topic>Liver Cirrhosis, Experimental - pathology</topic><topic>Lung - enzymology</topic><topic>Lung - pathology</topic><topic>Male</topic><topic>Oxidative Stress</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Superoxide Dismutase - metabolism</topic><topic>Thiobarbituric Acid Reactive Substances - metabolism</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Salatti Ferrari, Renata</creatorcontrib><creatorcontrib>da Rosa, Darlan Pase</creatorcontrib><creatorcontrib>Forgiarini, Luiz Felipe</creatorcontrib><creatorcontrib>Bona, Sílvia</creatorcontrib><creatorcontrib>Simões Dias, Alexandre</creatorcontrib><creatorcontrib>Marroni, Norma Anair Possa</creatorcontrib><collection>الدوريات العلمية والإحصائية - e-Marefa Academic and Statistical Periodicals</collection><collection>معرفة - المحتوى العربي الأكاديمي المتكامل - e-Marefa Academic Complete</collection><collection>Hindawi Publishing Complete</collection><collection>Hindawi Publishing Subscription Journals</collection><collection>Hindawi Publishing Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Oxidative medicine and cellular longevity</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Salatti Ferrari, Renata</au><au>da Rosa, Darlan Pase</au><au>Forgiarini, Luiz Felipe</au><au>Bona, Sílvia</au><au>Simões Dias, Alexandre</au><au>Marroni, Norma Anair Possa</au><au>Tirosh, Oren</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Oxidative Stress and Pulmonary Changes in Experimental Liver Cirrhosis</atitle><jtitle>Oxidative medicine and cellular longevity</jtitle><addtitle>Oxid Med Cell Longev</addtitle><date>2012-01-01</date><risdate>2012</risdate><volume>2012</volume><issue>2012</issue><spage>1</spage><epage>8</epage><pages>1-8</pages><issn>1942-0900</issn><eissn>1942-0994</eissn><abstract>The use of carbon tetrachloride (CCl4) in rats is an experimental model of hepatic tissue damage; which leads to fibrosis, and at the long term, cirrhosis. Cirrhosis is the consequence of progressive continued liver damage, it may be reversible when the damaging noxae have been withdrawn. The aim of this study is to evaluate the changes caused by cirrhosis in lung and liver, through the experimental model of intraperitoneal CCI4 administration. We used 18 male Wistar rats divided into three groups: control (CO) and two groups divided by the time of cirrhosis induction by CCI4: G1 (11 weeks), G2 (16 weeks). We found significant increase of transaminase levels and lipid peroxidation (TBARS) in liver and lung tissue and also increased antioxidant enzymes SOD and CAT, as well as the expression of TNF-α and IL-1β in the lung of cirrhotic animals. We observed changes in gas exchange in both cirrhotic groups. We can conclude that our model reproduces a model of liver cirrhosis, which causes alterations in the pulmonary system that leads to changes in gas exchange and size of pulmonary vessels.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Puplishing Corporation</pub><pmid>23316268</pmid><doi>10.1155/2012/486190</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Arteries - metabolism Blood Gas Analysis Catalase - metabolism Interleukin-1beta - metabolism Liver - enzymology Liver - pathology Liver Cirrhosis, Experimental - pathology Lung - enzymology Lung - pathology Male Oxidative Stress Rats Rats, Wistar Superoxide Dismutase - metabolism Thiobarbituric Acid Reactive Substances - metabolism Tumor Necrosis Factor-alpha - metabolism |
| title | Oxidative Stress and Pulmonary Changes in Experimental Liver Cirrhosis |
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