S-nitroso-N-acetylcysteine ameliorates ischemia-reperfusion injury in the steatotic liver

Detalhes bibliográficos
Autor(a) principal: Andraus, Wellington
Data de Publicação: 2010
Outros Autores: Souza, Gabriela Freitas Pereira de, Oliveira, Marcelo Ganzarolli de, Haddad, Luciana B. P., Coelho, Ana Maria M., Galvão, Flavio Henrique, Leitão, Regina Maria Cubero, D'Albuquerque, Luiz Augusto Carneiro, Machado, Marcel Cerqueira Cesar
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Clinics
Texto Completo: https://www.revistas.usp.br/clinics/article/view/18341
Resumo: BACKGROUND: Steatosis is currently the most common chronic liver disease and it can aggravate ischemia-reperfusion (IR) lesions. We hypothesized that S-nitroso-N-acetylcysteine (SNAC), an NO donor component, can ameliorate cell damage from IR injury. In this paper, we report the effect of SNAC on liver IR in rats with normal livers compared to those with steatotic livers. METHODS: Thirty-four rats were divided into five groups: I (n=8), IR in normal liver; II (n=8), IR in normal liver with SNAC; III (n=9), IR in steatotic liver; IV (n=9), IR in steatotic liver with SNAC; and V (n=10), SHAN. Liver steatosis was achieved by administration of a protein-free diet. A SNAC solution was infused intraperitoneally for one hour, beginning 30 min. after partial (70%) liver ischemia. The volume of solution infused was 1 ml/100 g body weight. The animals were sacrificed four hours after reperfusion, and the liver and lung were removed for analysis. We assessed hepatic histology, mitochondrial respiration, oxidative stress (MDA), and pulmonary myeloperoxidase. RESULTS: All groups showed significant alterations compared with the group that received SHAN. The results from the steatotic SNAC group revealed a significant improvement in liver mitochondrial respiration and oxidative stress compared to the steatotic group without SNAC. No difference in myeloperoxidase was observed. Histological analysis revealed no difference between the non-steatotic groups. However, the SNAC groups showed less intraparenchymal hemorrhage than groups without SNAC (p=0.02). CONCLUSION: This study suggests that SNAC effectively protects against IR injury in the steatotic liver but not in the normal liver.
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spelling S-nitroso-N-acetylcysteine ameliorates ischemia-reperfusion injury in the steatotic liver Fatty liverS-nitrosothiolS-nitroso-N-acetylcysteinereperfusion injuryoxidative stress BACKGROUND: Steatosis is currently the most common chronic liver disease and it can aggravate ischemia-reperfusion (IR) lesions. We hypothesized that S-nitroso-N-acetylcysteine (SNAC), an NO donor component, can ameliorate cell damage from IR injury. In this paper, we report the effect of SNAC on liver IR in rats with normal livers compared to those with steatotic livers. METHODS: Thirty-four rats were divided into five groups: I (n=8), IR in normal liver; II (n=8), IR in normal liver with SNAC; III (n=9), IR in steatotic liver; IV (n=9), IR in steatotic liver with SNAC; and V (n=10), SHAN. Liver steatosis was achieved by administration of a protein-free diet. A SNAC solution was infused intraperitoneally for one hour, beginning 30 min. after partial (70%) liver ischemia. The volume of solution infused was 1 ml/100 g body weight. The animals were sacrificed four hours after reperfusion, and the liver and lung were removed for analysis. We assessed hepatic histology, mitochondrial respiration, oxidative stress (MDA), and pulmonary myeloperoxidase. RESULTS: All groups showed significant alterations compared with the group that received SHAN. The results from the steatotic SNAC group revealed a significant improvement in liver mitochondrial respiration and oxidative stress compared to the steatotic group without SNAC. No difference in myeloperoxidase was observed. Histological analysis revealed no difference between the non-steatotic groups. However, the SNAC groups showed less intraparenchymal hemorrhage than groups without SNAC (p=0.02). CONCLUSION: This study suggests that SNAC effectively protects against IR injury in the steatotic liver but not in the normal liver. Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo2010-01-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionapplication/pdfhttps://www.revistas.usp.br/clinics/article/view/1834110.1590/S1807-59322010000700011Clinics; Vol. 65 No. 7 (2010); 715-721 Clinics; v. 65 n. 7 (2010); 715-721 Clinics; Vol. 65 Núm. 7 (2010); 715-721 1980-53221807-5932reponame:Clinicsinstname:Universidade de São Paulo (USP)instacron:USPenghttps://www.revistas.usp.br/clinics/article/view/18341/20404Andraus, WellingtonSouza, Gabriela Freitas Pereira deOliveira, Marcelo Ganzarolli deHaddad, Luciana B. P.Coelho, Ana Maria M.Galvão, Flavio HenriqueLeitão, Regina Maria CuberoD'Albuquerque, Luiz Augusto CarneiroMachado, Marcel Cerqueira Cesarinfo:eu-repo/semantics/openAccess2012-05-23T11:14:54Zoai:revistas.usp.br:article/18341Revistahttps://www.revistas.usp.br/clinicsPUBhttps://www.revistas.usp.br/clinics/oai||clinics@hc.fm.usp.br1980-53221807-5932opendoar:2012-05-23T11:14:54Clinics - Universidade de São Paulo (USP)false
dc.title.none.fl_str_mv S-nitroso-N-acetylcysteine ameliorates ischemia-reperfusion injury in the steatotic liver
title S-nitroso-N-acetylcysteine ameliorates ischemia-reperfusion injury in the steatotic liver
spellingShingle S-nitroso-N-acetylcysteine ameliorates ischemia-reperfusion injury in the steatotic liver
Andraus, Wellington
Fatty liver
S-nitrosothiol
S-nitroso-N-acetylcysteine
reperfusion injury
oxidative stress
title_short S-nitroso-N-acetylcysteine ameliorates ischemia-reperfusion injury in the steatotic liver
title_full S-nitroso-N-acetylcysteine ameliorates ischemia-reperfusion injury in the steatotic liver
title_fullStr S-nitroso-N-acetylcysteine ameliorates ischemia-reperfusion injury in the steatotic liver
title_full_unstemmed S-nitroso-N-acetylcysteine ameliorates ischemia-reperfusion injury in the steatotic liver
title_sort S-nitroso-N-acetylcysteine ameliorates ischemia-reperfusion injury in the steatotic liver
author Andraus, Wellington
author_facet Andraus, Wellington
Souza, Gabriela Freitas Pereira de
Oliveira, Marcelo Ganzarolli de
Haddad, Luciana B. P.
Coelho, Ana Maria M.
Galvão, Flavio Henrique
Leitão, Regina Maria Cubero
D'Albuquerque, Luiz Augusto Carneiro
Machado, Marcel Cerqueira Cesar
author_role author
author2 Souza, Gabriela Freitas Pereira de
Oliveira, Marcelo Ganzarolli de
Haddad, Luciana B. P.
Coelho, Ana Maria M.
Galvão, Flavio Henrique
Leitão, Regina Maria Cubero
D'Albuquerque, Luiz Augusto Carneiro
Machado, Marcel Cerqueira Cesar
author2_role author
author
author
author
author
author
author
author
dc.contributor.author.fl_str_mv Andraus, Wellington
Souza, Gabriela Freitas Pereira de
Oliveira, Marcelo Ganzarolli de
Haddad, Luciana B. P.
Coelho, Ana Maria M.
Galvão, Flavio Henrique
Leitão, Regina Maria Cubero
D'Albuquerque, Luiz Augusto Carneiro
Machado, Marcel Cerqueira Cesar
dc.subject.por.fl_str_mv Fatty liver
S-nitrosothiol
S-nitroso-N-acetylcysteine
reperfusion injury
oxidative stress
topic Fatty liver
S-nitrosothiol
S-nitroso-N-acetylcysteine
reperfusion injury
oxidative stress
description BACKGROUND: Steatosis is currently the most common chronic liver disease and it can aggravate ischemia-reperfusion (IR) lesions. We hypothesized that S-nitroso-N-acetylcysteine (SNAC), an NO donor component, can ameliorate cell damage from IR injury. In this paper, we report the effect of SNAC on liver IR in rats with normal livers compared to those with steatotic livers. METHODS: Thirty-four rats were divided into five groups: I (n=8), IR in normal liver; II (n=8), IR in normal liver with SNAC; III (n=9), IR in steatotic liver; IV (n=9), IR in steatotic liver with SNAC; and V (n=10), SHAN. Liver steatosis was achieved by administration of a protein-free diet. A SNAC solution was infused intraperitoneally for one hour, beginning 30 min. after partial (70%) liver ischemia. The volume of solution infused was 1 ml/100 g body weight. The animals were sacrificed four hours after reperfusion, and the liver and lung were removed for analysis. We assessed hepatic histology, mitochondrial respiration, oxidative stress (MDA), and pulmonary myeloperoxidase. RESULTS: All groups showed significant alterations compared with the group that received SHAN. The results from the steatotic SNAC group revealed a significant improvement in liver mitochondrial respiration and oxidative stress compared to the steatotic group without SNAC. No difference in myeloperoxidase was observed. Histological analysis revealed no difference between the non-steatotic groups. However, the SNAC groups showed less intraparenchymal hemorrhage than groups without SNAC (p=0.02). CONCLUSION: This study suggests that SNAC effectively protects against IR injury in the steatotic liver but not in the normal liver.
publishDate 2010
dc.date.none.fl_str_mv 2010-01-01
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.uri.fl_str_mv https://www.revistas.usp.br/clinics/article/view/18341
10.1590/S1807-59322010000700011
url https://www.revistas.usp.br/clinics/article/view/18341
identifier_str_mv 10.1590/S1807-59322010000700011
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv https://www.revistas.usp.br/clinics/article/view/18341/20404
dc.rights.driver.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo
publisher.none.fl_str_mv Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo
dc.source.none.fl_str_mv Clinics; Vol. 65 No. 7 (2010); 715-721
Clinics; v. 65 n. 7 (2010); 715-721
Clinics; Vol. 65 Núm. 7 (2010); 715-721
1980-5322
1807-5932
reponame:Clinics
instname:Universidade de São Paulo (USP)
instacron:USP
instname_str Universidade de São Paulo (USP)
instacron_str USP
institution USP
reponame_str Clinics
collection Clinics
repository.name.fl_str_mv Clinics - Universidade de São Paulo (USP)
repository.mail.fl_str_mv ||clinics@hc.fm.usp.br
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