Beta-glucan prevents toxic effects of 2,3,7,8-TCDD in terms of oxidative and histopathological damage in heart tissue of rats
Autor(a) principal: | |
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Data de Publicação: | 2018 |
Outros Autores: | , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Brazilian Journal of Pharmaceutical Sciences |
Texto Completo: | https://www.revistas.usp.br/bjps/article/view/153868 |
Resumo: | 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a widespread environmental contaminant which causes severe toxic effects. Despite there is some suggestion concerning with TCDD induced cardiotoxicity such as formation of free radicals, the main mechanism has not been entirely explained. Beta-glucan is known as strong antioxidant matter and can scavenge free radicals. Therefore this study aimed to investigate the protective effects of beta-glucan against TCDD induced cardiotoxicity in rats. In this study, 2-3 months of age and 190-250 g in weight 32 rats were randomly divided into four equal groups (n=8 for each group). Group 1 was control; Group 2 was TCDD group (2 µg/kg/week); group 3 was the beta-glucan group(50 mg/kg/day), and group 4 was TCDD and beta-glucan treatment group. The heart samples were taken from rats after 21 days treatment. The results were shown that Despite TCDD exposure visibly caused to increase (p ≤ 0.001) in TBARS levels, It caused a visible decline in the levels of GSH, CAT, GSH-Px, and SOD. However Beta glucan significantly increased GSH, CAT, GSH-Px, SOD levels and decreased generation of TBARS. Additionally, our histopathological observations were in agreement with the biochemical results. In conclusion, Beta-glucan treatment exhibited protective activity on TCDD induced cardiotoxicity. |
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Brazilian Journal of Pharmaceutical Sciences |
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Beta-glucan prevents toxic effects of 2,3,7,8-TCDD in terms of oxidative and histopathological damage in heart tissue of ratsBeta-glucan/protective effects2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD)CardiotoxicityRats2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a widespread environmental contaminant which causes severe toxic effects. Despite there is some suggestion concerning with TCDD induced cardiotoxicity such as formation of free radicals, the main mechanism has not been entirely explained. Beta-glucan is known as strong antioxidant matter and can scavenge free radicals. Therefore this study aimed to investigate the protective effects of beta-glucan against TCDD induced cardiotoxicity in rats. In this study, 2-3 months of age and 190-250 g in weight 32 rats were randomly divided into four equal groups (n=8 for each group). Group 1 was control; Group 2 was TCDD group (2 µg/kg/week); group 3 was the beta-glucan group(50 mg/kg/day), and group 4 was TCDD and beta-glucan treatment group. The heart samples were taken from rats after 21 days treatment. The results were shown that Despite TCDD exposure visibly caused to increase (p ≤ 0.001) in TBARS levels, It caused a visible decline in the levels of GSH, CAT, GSH-Px, and SOD. However Beta glucan significantly increased GSH, CAT, GSH-Px, SOD levels and decreased generation of TBARS. Additionally, our histopathological observations were in agreement with the biochemical results. In conclusion, Beta-glucan treatment exhibited protective activity on TCDD induced cardiotoxicity.Universidade de São Paulo. Faculdade de Ciências Farmacêuticas2018-11-29info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionapplication/pdfhttps://www.revistas.usp.br/bjps/article/view/15386810.1590/s2175-97902018000317674Brazilian Journal of Pharmaceutical Sciences; Vol. 54 Núm. 3 (2018); e17674Brazilian Journal of Pharmaceutical Sciences; v. 54 n. 3 (2018); e17674Brazilian Journal of Pharmaceutical Sciences; Vol. 54 No. 3 (2018); e176742175-97901984-8250reponame:Brazilian Journal of Pharmaceutical Sciencesinstname:Universidade de São Paulo (USP)instacron:USPenghttps://www.revistas.usp.br/bjps/article/view/153868/150220Copyright (c) 2018 Brazilian Journal of Pharmaceutical Sciences (Impresso)info:eu-repo/semantics/openAccessCiftci, OsmanDuman, Ahmet SefaTurkmen, Neşe BasakTaslıdere, Aslı2019-03-17T13:18:44Zoai:revistas.usp.br:article/153868Revistahttps://www.revistas.usp.br/bjps/indexPUBhttps://old.scielo.br/oai/scielo-oai.phpbjps@usp.br||elizabeth.igne@gmail.com2175-97901984-8250opendoar:2019-03-17T13:18:44Brazilian Journal of Pharmaceutical Sciences - Universidade de São Paulo (USP)false |
dc.title.none.fl_str_mv |
Beta-glucan prevents toxic effects of 2,3,7,8-TCDD in terms of oxidative and histopathological damage in heart tissue of rats |
title |
Beta-glucan prevents toxic effects of 2,3,7,8-TCDD in terms of oxidative and histopathological damage in heart tissue of rats |
spellingShingle |
Beta-glucan prevents toxic effects of 2,3,7,8-TCDD in terms of oxidative and histopathological damage in heart tissue of rats Ciftci, Osman Beta-glucan/protective effects 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) Cardiotoxicity Rats |
title_short |
Beta-glucan prevents toxic effects of 2,3,7,8-TCDD in terms of oxidative and histopathological damage in heart tissue of rats |
title_full |
Beta-glucan prevents toxic effects of 2,3,7,8-TCDD in terms of oxidative and histopathological damage in heart tissue of rats |
title_fullStr |
Beta-glucan prevents toxic effects of 2,3,7,8-TCDD in terms of oxidative and histopathological damage in heart tissue of rats |
title_full_unstemmed |
Beta-glucan prevents toxic effects of 2,3,7,8-TCDD in terms of oxidative and histopathological damage in heart tissue of rats |
title_sort |
Beta-glucan prevents toxic effects of 2,3,7,8-TCDD in terms of oxidative and histopathological damage in heart tissue of rats |
author |
Ciftci, Osman |
author_facet |
Ciftci, Osman Duman, Ahmet Sefa Turkmen, Neşe Basak Taslıdere, Aslı |
author_role |
author |
author2 |
Duman, Ahmet Sefa Turkmen, Neşe Basak Taslıdere, Aslı |
author2_role |
author author author |
dc.contributor.author.fl_str_mv |
Ciftci, Osman Duman, Ahmet Sefa Turkmen, Neşe Basak Taslıdere, Aslı |
dc.subject.por.fl_str_mv |
Beta-glucan/protective effects 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) Cardiotoxicity Rats |
topic |
Beta-glucan/protective effects 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) Cardiotoxicity Rats |
description |
2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a widespread environmental contaminant which causes severe toxic effects. Despite there is some suggestion concerning with TCDD induced cardiotoxicity such as formation of free radicals, the main mechanism has not been entirely explained. Beta-glucan is known as strong antioxidant matter and can scavenge free radicals. Therefore this study aimed to investigate the protective effects of beta-glucan against TCDD induced cardiotoxicity in rats. In this study, 2-3 months of age and 190-250 g in weight 32 rats were randomly divided into four equal groups (n=8 for each group). Group 1 was control; Group 2 was TCDD group (2 µg/kg/week); group 3 was the beta-glucan group(50 mg/kg/day), and group 4 was TCDD and beta-glucan treatment group. The heart samples were taken from rats after 21 days treatment. The results were shown that Despite TCDD exposure visibly caused to increase (p ≤ 0.001) in TBARS levels, It caused a visible decline in the levels of GSH, CAT, GSH-Px, and SOD. However Beta glucan significantly increased GSH, CAT, GSH-Px, SOD levels and decreased generation of TBARS. Additionally, our histopathological observations were in agreement with the biochemical results. In conclusion, Beta-glucan treatment exhibited protective activity on TCDD induced cardiotoxicity. |
publishDate |
2018 |
dc.date.none.fl_str_mv |
2018-11-29 |
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/bjps/article/view/153868 10.1590/s2175-97902018000317674 |
url |
https://www.revistas.usp.br/bjps/article/view/153868 |
identifier_str_mv |
10.1590/s2175-97902018000317674 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
https://www.revistas.usp.br/bjps/article/view/153868/150220 |
dc.rights.driver.fl_str_mv |
Copyright (c) 2018 Brazilian Journal of Pharmaceutical Sciences (Impresso) info:eu-repo/semantics/openAccess |
rights_invalid_str_mv |
Copyright (c) 2018 Brazilian Journal of Pharmaceutical Sciences (Impresso) |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
application/pdf |
dc.publisher.none.fl_str_mv |
Universidade de São Paulo. Faculdade de Ciências Farmacêuticas |
publisher.none.fl_str_mv |
Universidade de São Paulo. Faculdade de Ciências Farmacêuticas |
dc.source.none.fl_str_mv |
Brazilian Journal of Pharmaceutical Sciences; Vol. 54 Núm. 3 (2018); e17674 Brazilian Journal of Pharmaceutical Sciences; v. 54 n. 3 (2018); e17674 Brazilian Journal of Pharmaceutical Sciences; Vol. 54 No. 3 (2018); e17674 2175-9790 1984-8250 reponame:Brazilian Journal of Pharmaceutical Sciences instname:Universidade de São Paulo (USP) instacron:USP |
instname_str |
Universidade de São Paulo (USP) |
instacron_str |
USP |
institution |
USP |
reponame_str |
Brazilian Journal of Pharmaceutical Sciences |
collection |
Brazilian Journal of Pharmaceutical Sciences |
repository.name.fl_str_mv |
Brazilian Journal of Pharmaceutical Sciences - Universidade de São Paulo (USP) |
repository.mail.fl_str_mv |
bjps@usp.br||elizabeth.igne@gmail.com |
_version_ |
1800222913811447808 |