Efeitos da administração do disseleneto de difenila sobre o dano hepático induzido por 2-nitropropano, cádmio e tetracloreto de carbono
Ano de defesa: | 2008 |
---|---|
Autor(a) principal: | |
Orientador(a): | |
Banca de defesa: | , , , |
Tipo de documento: | Tese |
Tipo de acesso: | Acesso aberto |
Idioma: | por |
Instituição de defesa: |
Universidade Federal de Santa Maria
|
Programa de Pós-Graduação: |
Programa de Pós-Graduação em Ciências Biológicas: Bioquímica Toxicológica
|
Departamento: |
Bioquímica
|
País: |
BR
|
Palavras-chave em Português: | |
Palavras-chave em Inglês: | |
Área do conhecimento CNPq: | |
Link de acesso: | http://repositorio.ufsm.br/handle/1/4396 |
Resumo: | The liver presented exceptional characteristics, like controlling energy production, immunological defenses, and blood reserve. In the environment like in the work place, the human is exposed to a different kind of hepatotoxic compounds, for example, on inks and derivatives (2-nitropropane), chemical reagents (carbon tetrachloride) and in tobacco smoke (2-nitropropane and cadmium). In fact, is interesting studies of therapies which protect or ameliorated the damage induced by these compounds. Considering the growing interesting around organochalcogens, in special interest, diphenyl diselenide (PhSe)2, which posses important pharmacological properties, such as: anti-ulcer, antiinflammatory, antinociceptive, anti-hyperglycemic, protected against orofacial diskinesia induced by reserpine and halopheridol and may act on memory facilitation in mice, the hepatoprotective properties of this compound induced by different models of liver damage (2-nitropropane, cadmium and carbon tetrachloride) were examined. The results demonstrated that (PhSe)2 (100 µmol/kg) significantly reduced hepatic markers levels when compared to 2-nitropropane (2-NP) group. Treatment with diphenyl diselenide, at all doses, effectively protects against the increase of lipid peroxidation when compared to 2-NP group. In addition, histological examination revealed that 2-NP treatment causes a moderate swelling and degenerative alterations on hepatocytes and (PhSe)2 protects against these alterations. This study evidences the protective effect of diphenyl diselenide by 2-NP-induced acute hepatic damage. In addition the effect of post-treatment with (PhSe)2 on liver damage induced by 2-NP was also examined. (PhSe)2 effectively restored the increase of aminotransferase activities and urea level when compared to the 2-NP group. At the highest dose (100 mol/kg), (PhSe)2 decreased -glutamyl transferase activity (GGT) and ameliorated the increase of hepatic and renal lipid peroxidation when compared to 2-NP group. 2-NP reduced catalase activity (CAT) and did not alter superoxide dismutase activity (SOD) nor ascorbic acid level. This study points out the involvement of CAT activity in 2-NP-induced acute liver damage and suggests that the post-treatment with diphenyl diselenide was effective in restoring the hepatic damage induced by 2-NP. Similar results were obtained with cadmium (Cd), an environmental toxic metal implicated in human diseases. Cadmium content determined in the tissue of rats exposed to cadmium chloride (CdCl2) provides evidence that the liver is the major cadmium target. The concentration of cadmium in liver was about three fold higher than that in kidney, and (PhSe)2 reduced about six fold the levels of this metal in liver of rats exposed. Rats exposed to CdCl2 showed histological alterations abolished by (PhSe)2 administration. In addition, (PhSe)2 administration ameliorated plasma malondialdehyde (MDA) levels, aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), lactate dehydrogenase (LDH) and GGT activities increased by CdCl2 exposure. In conclusion, this study demonstrated that co-treatment with (PhSe)2 ameliorated hepatotoxicity and cellular damage in rat liver after sub-chronic exposure with CdCl2. The proposed mechanisms by which (PhSe)2 acts in this experimental protocol are its antioxidant properties and its capacity to form a complex with Cd. On the contrary, the administration of (PhSe)2 potentiated acute hepatic damage induced by carbon tetrachloride (CCl4), as manifested by an increase in biochemical parameters (AST, ALT, ALP, GGT and BT) and severe alteration in histopathology. This study also demonstrated a potentiation of lipid peroxidation levels and a consequent depletion of important antioxidant defenses including catalase and ascorbic acid, suggesting that the oxidative damage is related to the potentiation effect induced by (PhSe)2. Considering the results obtained, could be suggested that (PhSe)2 present a hepatoprotective effect depending of experimental protocol. |
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2017-04-242017-04-242008-02-01BORGES, Lysandro Pinto. Effects of diphenyl diselenide administration on liver damage induced by 2-nitropropane, cadmium and carbon tetrachloride. 2008. 126 f. Tese (Doutorado em Bioquímica) - Universidade Federal de Santa Maria, Santa Maria, 2008.http://repositorio.ufsm.br/handle/1/4396The liver presented exceptional characteristics, like controlling energy production, immunological defenses, and blood reserve. In the environment like in the work place, the human is exposed to a different kind of hepatotoxic compounds, for example, on inks and derivatives (2-nitropropane), chemical reagents (carbon tetrachloride) and in tobacco smoke (2-nitropropane and cadmium). In fact, is interesting studies of therapies which protect or ameliorated the damage induced by these compounds. Considering the growing interesting around organochalcogens, in special interest, diphenyl diselenide (PhSe)2, which posses important pharmacological properties, such as: anti-ulcer, antiinflammatory, antinociceptive, anti-hyperglycemic, protected against orofacial diskinesia induced by reserpine and halopheridol and may act on memory facilitation in mice, the hepatoprotective properties of this compound induced by different models of liver damage (2-nitropropane, cadmium and carbon tetrachloride) were examined. The results demonstrated that (PhSe)2 (100 µmol/kg) significantly reduced hepatic markers levels when compared to 2-nitropropane (2-NP) group. Treatment with diphenyl diselenide, at all doses, effectively protects against the increase of lipid peroxidation when compared to 2-NP group. In addition, histological examination revealed that 2-NP treatment causes a moderate swelling and degenerative alterations on hepatocytes and (PhSe)2 protects against these alterations. This study evidences the protective effect of diphenyl diselenide by 2-NP-induced acute hepatic damage. In addition the effect of post-treatment with (PhSe)2 on liver damage induced by 2-NP was also examined. (PhSe)2 effectively restored the increase of aminotransferase activities and urea level when compared to the 2-NP group. At the highest dose (100 mol/kg), (PhSe)2 decreased -glutamyl transferase activity (GGT) and ameliorated the increase of hepatic and renal lipid peroxidation when compared to 2-NP group. 2-NP reduced catalase activity (CAT) and did not alter superoxide dismutase activity (SOD) nor ascorbic acid level. This study points out the involvement of CAT activity in 2-NP-induced acute liver damage and suggests that the post-treatment with diphenyl diselenide was effective in restoring the hepatic damage induced by 2-NP. Similar results were obtained with cadmium (Cd), an environmental toxic metal implicated in human diseases. Cadmium content determined in the tissue of rats exposed to cadmium chloride (CdCl2) provides evidence that the liver is the major cadmium target. The concentration of cadmium in liver was about three fold higher than that in kidney, and (PhSe)2 reduced about six fold the levels of this metal in liver of rats exposed. Rats exposed to CdCl2 showed histological alterations abolished by (PhSe)2 administration. In addition, (PhSe)2 administration ameliorated plasma malondialdehyde (MDA) levels, aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), lactate dehydrogenase (LDH) and GGT activities increased by CdCl2 exposure. In conclusion, this study demonstrated that co-treatment with (PhSe)2 ameliorated hepatotoxicity and cellular damage in rat liver after sub-chronic exposure with CdCl2. The proposed mechanisms by which (PhSe)2 acts in this experimental protocol are its antioxidant properties and its capacity to form a complex with Cd. On the contrary, the administration of (PhSe)2 potentiated acute hepatic damage induced by carbon tetrachloride (CCl4), as manifested by an increase in biochemical parameters (AST, ALT, ALP, GGT and BT) and severe alteration in histopathology. This study also demonstrated a potentiation of lipid peroxidation levels and a consequent depletion of important antioxidant defenses including catalase and ascorbic acid, suggesting that the oxidative damage is related to the potentiation effect induced by (PhSe)2. Considering the results obtained, could be suggested that (PhSe)2 present a hepatoprotective effect depending of experimental protocol.O fígado apresenta extraordinária pluralidade funcional, destacando-se no controle de produção de energia, defesa imunológica e reserva volêmica. No meio ambiente e ocupacionalmente, o ser humano está exposto a uma variedade de compostos hepatotóxicos, como por exemplo, no uso de tintas e seus derivados (2-nitropropano), reagentes químicos (tetracloreto de carbono) e na exposição ao cigarro (cádmio e 2-nitropropano). Portanto, é interessante o estudo de terapias que previnam ou até mesmo revertam à intoxicação causada por estes compostos. Considerando o crescente interesse por compostos orgânicos de selênio, em especial o disseleneto de difenila ((PhSe)2) que possui propriedades farmacológicas mais amplas como: efeitos anti-úlcera, antiinflamatório e antinociceptivo, anti- hiperglicemiante, protege contra a discinesia orofacial induzida por reserpina e haloperidol e pode atuar na facilitação da formação de memória em camundongos. Deste modo, os efeitos hepatoprotetores deste composto frente a diferentes modelos de dano hepático (2-nitropropano, cádmio e tetracloreto de carbono) foram examinados. Os resultados obtidos neste estudo demonstraram que a administração de (PhSe)2 (100 µmol/kg) reduziu os níveis de marcadores hepáticos e os níveis de peroxidação lipídica quando comparado ao grupo tratado com 2-nitropropano (2-NP). Além disso, os exames histológicos revelaram que o tratamento com 2-NP causou alterações degenerativas nos hepatócitos e que o (PhSe)2 foi capaz de proteger, evidenciando o efeito hepatoprotetor desse composto sobre o dano hepático induzido por 2-NP. O efeito do pós-tratamento com (PhSe)2 sobre o dano hepático induzido com 2-NP também foi investigado. Este composto restaurou a atividade plasmática das enzimas aminotransferases e os níveis de uréia quando comparado ao grupo tratado com 2-NP. Na maior dose (100 mol/kg), o (PhSe)2 causou uma diminuição na atividade da enzima -glutamil transferase (GGT) e restituiu o aumento nos níveis de peroxidação lipídica hepáticos e renais quando comparado ao grupo tratado com 2-NP. O tratamento com 2-NP reduziu a atividade hepática da catalase, entretanto não alterou a atividade da superóxido dismutase (SOD) e os níveis de ácido ascórbico, sugerindo que a inibição da CAT pode estar relacionada com o aumento nos níveis de peroxidação lipídica hepática nos ratos tratados com 2-NP. Resultados similares foram encontrados quando o dano hepático foi induzido por cádmio (Cd), um contaminante ambiental implicado em várias doenças. O conteúdo de Cd determinado nos ratos expostos ao cloreto de cádmio (CdCl2) provêm evidências de que o fígado é o maior alvo da toxicidade deste metal. A concentração de cádmio no fígado foi em torno de 3 vezes maiores que os níveis encontrados no rim. O (PhSe)2 reduziu em torno de 6 vezes os níveis deste metal no fígado dos ratos expostos ao CdCl2. Além disso, a administração de (PhSe)2 causou uma redução nos níveis de malondialdeído plasmáticos (MDA), na atividade das aminotransferases, na fosfatase alcalina (ALP), lactato desidrogenase (LDH) e GGT quando comparado ao grupo tratado com cádmio. Em conclusão, esse estudo demonstrou que o tratamento concomitante com (PhSe)2 reduziu a hepatotoxicidade e o dano celular em fígado de ratos expostos ao cádmio. O mecanismo proposto para ação do (PhSe)2 pode ser devido as suas propriedades antioxidantes ou pela sua capacidade de formar um complexo com Cd. Em contraste, a administração de (PhSe)2 potencializou o dano induzido por tetracloreto de carbono (CCl4), o que foi demonstrado pelo aumento dos níveis de marcadores bioquímicos (AST, ALT, ALP, GGT and BT) e pela severa alteração na histologia. Esses estudos também demonstraram que a administração de (PhSe)2 potencializou os níveis de peroxidação lipídica com consequente depleção das defesas antioxidantes, como a catalase e o ácido ascórbico, sugerindo que o dano oxidativo está relacionado com este efeito. Considerando os resultados obtidos, podemos sugerir que o disseleneto de difenila apresenta um efeito hepatoprotetor dependendo do modelo experimental.application/pdfporUniversidade Federal de Santa MariaPrograma de Pós-Graduação em Ciências Biológicas: Bioquímica ToxicológicaUFSMBRBioquímicaDano hepáticoSelênioDisseleneto de difenilaTetracloreto de carbonoCádmio2-nitropropanoLiver damageSeleniumDiphenyl diselenideCarbon tetrachlorideCadmium2-nitropropaneCNPQ::CIENCIAS BIOLOGICAS::BIOQUIMICAEfeitos da administração do disseleneto de difenila sobre o dano hepático induzido por 2-nitropropano, cádmio e tetracloreto de carbonoEffects of diphenyl diselenide administration on liver damage induced by 2-nitropropane, cadmium and carbon tetrachlorideinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/doctoralThesisZeni, Gilson Rogériohttp://lattes.cnpq.br/2355575631197937Nogueira, Cristina Waynehttp://lattes.cnpq.br/2877042401245169Garcia, Solange Cristinahttp://lattes.cnpq.br/6687355709603379Lago, Lissandra Dalhttp://lattes.cnpq.br/7448358134461750Baldisserotto, Bernardohttp://lattes.cnpq.br/1036046601275319Mazzanti, Alexandrehttp://lattes.cnpq.br/3504517995843014http://lattes.cnpq.br/5015405877622893Borges, Lysandro Pinto200800000002400500300300500300300500b21a898a-0ab0-4f33-b980-2b55ef590b94da80830a-2408-4fe4-be81-a00e16a1c4c5c2b1a64f-5f22-4779-9732-0c543f42b42d08641410-3b67-4735-9a1f-8563f344fcd6d24ae8c7-9b57-495d-95a9-a11c8afb4d79b8794c26-5128-41cb-80bc-62b6530f3dee507e6b84-7078-432e-93a3-22ebb903596binfo:eu-repo/semantics/openAccessreponame:Biblioteca Digital de Teses e Dissertações do UFSMinstname:Universidade Federal de Santa Maria (UFSM)instacron:UFSMORIGINALLYSANDROBORGES.pdfapplication/pdf4043898http://repositorio.ufsm.br/bitstream/1/4396/1/LYSANDROBORGES.pdf8fff2d38c56e91a2f83c5eb08a8ed955MD51TEXTLYSANDROBORGES.pdf.txtLYSANDROBORGES.pdf.txtExtracted texttext/plain130318http://repositorio.ufsm.br/bitstream/1/4396/2/LYSANDROBORGES.pdf.txta81a25b6d692a20aa6fc445709dc1166MD52THUMBNAILLYSANDROBORGES.pdf.jpgLYSANDROBORGES.pdf.jpgIM Thumbnailimage/jpeg6048http://repositorio.ufsm.br/bitstream/1/4396/3/LYSANDROBORGES.pdf.jpg791cfc6751d546de6c819971fbca3478MD531/43962023-04-17 10:13:30.965oai:repositorio.ufsm.br:1/4396Biblioteca Digital de Teses e Dissertaçõeshttps://repositorio.ufsm.br/ONGhttps://repositorio.ufsm.br/oai/requestatendimento.sib@ufsm.br||tedebc@gmail.comopendoar:2023-04-17T13:13:30Biblioteca Digital de Teses e Dissertações do UFSM - Universidade Federal de Santa Maria (UFSM)false |
dc.title.por.fl_str_mv |
Efeitos da administração do disseleneto de difenila sobre o dano hepático induzido por 2-nitropropano, cádmio e tetracloreto de carbono |
dc.title.alternative.eng.fl_str_mv |
Effects of diphenyl diselenide administration on liver damage induced by 2-nitropropane, cadmium and carbon tetrachloride |
title |
Efeitos da administração do disseleneto de difenila sobre o dano hepático induzido por 2-nitropropano, cádmio e tetracloreto de carbono |
spellingShingle |
Efeitos da administração do disseleneto de difenila sobre o dano hepático induzido por 2-nitropropano, cádmio e tetracloreto de carbono Borges, Lysandro Pinto Dano hepático Selênio Disseleneto de difenila Tetracloreto de carbono Cádmio 2-nitropropano Liver damage Selenium Diphenyl diselenide Carbon tetrachloride Cadmium 2-nitropropane CNPQ::CIENCIAS BIOLOGICAS::BIOQUIMICA |
title_short |
Efeitos da administração do disseleneto de difenila sobre o dano hepático induzido por 2-nitropropano, cádmio e tetracloreto de carbono |
title_full |
Efeitos da administração do disseleneto de difenila sobre o dano hepático induzido por 2-nitropropano, cádmio e tetracloreto de carbono |
title_fullStr |
Efeitos da administração do disseleneto de difenila sobre o dano hepático induzido por 2-nitropropano, cádmio e tetracloreto de carbono |
title_full_unstemmed |
Efeitos da administração do disseleneto de difenila sobre o dano hepático induzido por 2-nitropropano, cádmio e tetracloreto de carbono |
title_sort |
Efeitos da administração do disseleneto de difenila sobre o dano hepático induzido por 2-nitropropano, cádmio e tetracloreto de carbono |
author |
Borges, Lysandro Pinto |
author_facet |
Borges, Lysandro Pinto |
author_role |
author |
dc.contributor.advisor1.fl_str_mv |
Zeni, Gilson Rogério |
dc.contributor.advisor1Lattes.fl_str_mv |
http://lattes.cnpq.br/2355575631197937 |
dc.contributor.advisor-co1.fl_str_mv |
Nogueira, Cristina Wayne |
dc.contributor.advisor-co1Lattes.fl_str_mv |
http://lattes.cnpq.br/2877042401245169 |
dc.contributor.referee1.fl_str_mv |
Garcia, Solange Cristina |
dc.contributor.referee1Lattes.fl_str_mv |
http://lattes.cnpq.br/6687355709603379 |
dc.contributor.referee2.fl_str_mv |
Lago, Lissandra Dal |
dc.contributor.referee2Lattes.fl_str_mv |
http://lattes.cnpq.br/7448358134461750 |
dc.contributor.referee3.fl_str_mv |
Baldisserotto, Bernardo |
dc.contributor.referee3Lattes.fl_str_mv |
http://lattes.cnpq.br/1036046601275319 |
dc.contributor.referee4.fl_str_mv |
Mazzanti, Alexandre |
dc.contributor.referee4Lattes.fl_str_mv |
http://lattes.cnpq.br/3504517995843014 |
dc.contributor.authorLattes.fl_str_mv |
http://lattes.cnpq.br/5015405877622893 |
dc.contributor.author.fl_str_mv |
Borges, Lysandro Pinto |
contributor_str_mv |
Zeni, Gilson Rogério Nogueira, Cristina Wayne Garcia, Solange Cristina Lago, Lissandra Dal Baldisserotto, Bernardo Mazzanti, Alexandre |
dc.subject.por.fl_str_mv |
Dano hepático Selênio Disseleneto de difenila Tetracloreto de carbono Cádmio 2-nitropropano |
topic |
Dano hepático Selênio Disseleneto de difenila Tetracloreto de carbono Cádmio 2-nitropropano Liver damage Selenium Diphenyl diselenide Carbon tetrachloride Cadmium 2-nitropropane CNPQ::CIENCIAS BIOLOGICAS::BIOQUIMICA |
dc.subject.eng.fl_str_mv |
Liver damage Selenium Diphenyl diselenide Carbon tetrachloride Cadmium 2-nitropropane |
dc.subject.cnpq.fl_str_mv |
CNPQ::CIENCIAS BIOLOGICAS::BIOQUIMICA |
description |
The liver presented exceptional characteristics, like controlling energy production, immunological defenses, and blood reserve. In the environment like in the work place, the human is exposed to a different kind of hepatotoxic compounds, for example, on inks and derivatives (2-nitropropane), chemical reagents (carbon tetrachloride) and in tobacco smoke (2-nitropropane and cadmium). In fact, is interesting studies of therapies which protect or ameliorated the damage induced by these compounds. Considering the growing interesting around organochalcogens, in special interest, diphenyl diselenide (PhSe)2, which posses important pharmacological properties, such as: anti-ulcer, antiinflammatory, antinociceptive, anti-hyperglycemic, protected against orofacial diskinesia induced by reserpine and halopheridol and may act on memory facilitation in mice, the hepatoprotective properties of this compound induced by different models of liver damage (2-nitropropane, cadmium and carbon tetrachloride) were examined. The results demonstrated that (PhSe)2 (100 µmol/kg) significantly reduced hepatic markers levels when compared to 2-nitropropane (2-NP) group. Treatment with diphenyl diselenide, at all doses, effectively protects against the increase of lipid peroxidation when compared to 2-NP group. In addition, histological examination revealed that 2-NP treatment causes a moderate swelling and degenerative alterations on hepatocytes and (PhSe)2 protects against these alterations. This study evidences the protective effect of diphenyl diselenide by 2-NP-induced acute hepatic damage. In addition the effect of post-treatment with (PhSe)2 on liver damage induced by 2-NP was also examined. (PhSe)2 effectively restored the increase of aminotransferase activities and urea level when compared to the 2-NP group. At the highest dose (100 mol/kg), (PhSe)2 decreased -glutamyl transferase activity (GGT) and ameliorated the increase of hepatic and renal lipid peroxidation when compared to 2-NP group. 2-NP reduced catalase activity (CAT) and did not alter superoxide dismutase activity (SOD) nor ascorbic acid level. This study points out the involvement of CAT activity in 2-NP-induced acute liver damage and suggests that the post-treatment with diphenyl diselenide was effective in restoring the hepatic damage induced by 2-NP. Similar results were obtained with cadmium (Cd), an environmental toxic metal implicated in human diseases. Cadmium content determined in the tissue of rats exposed to cadmium chloride (CdCl2) provides evidence that the liver is the major cadmium target. The concentration of cadmium in liver was about three fold higher than that in kidney, and (PhSe)2 reduced about six fold the levels of this metal in liver of rats exposed. Rats exposed to CdCl2 showed histological alterations abolished by (PhSe)2 administration. In addition, (PhSe)2 administration ameliorated plasma malondialdehyde (MDA) levels, aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), lactate dehydrogenase (LDH) and GGT activities increased by CdCl2 exposure. In conclusion, this study demonstrated that co-treatment with (PhSe)2 ameliorated hepatotoxicity and cellular damage in rat liver after sub-chronic exposure with CdCl2. The proposed mechanisms by which (PhSe)2 acts in this experimental protocol are its antioxidant properties and its capacity to form a complex with Cd. On the contrary, the administration of (PhSe)2 potentiated acute hepatic damage induced by carbon tetrachloride (CCl4), as manifested by an increase in biochemical parameters (AST, ALT, ALP, GGT and BT) and severe alteration in histopathology. This study also demonstrated a potentiation of lipid peroxidation levels and a consequent depletion of important antioxidant defenses including catalase and ascorbic acid, suggesting that the oxidative damage is related to the potentiation effect induced by (PhSe)2. Considering the results obtained, could be suggested that (PhSe)2 present a hepatoprotective effect depending of experimental protocol. |
publishDate |
2008 |
dc.date.issued.fl_str_mv |
2008-02-01 |
dc.date.accessioned.fl_str_mv |
2017-04-24 |
dc.date.available.fl_str_mv |
2017-04-24 |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/doctoralThesis |
format |
doctoralThesis |
status_str |
publishedVersion |
dc.identifier.citation.fl_str_mv |
BORGES, Lysandro Pinto. Effects of diphenyl diselenide administration on liver damage induced by 2-nitropropane, cadmium and carbon tetrachloride. 2008. 126 f. Tese (Doutorado em Bioquímica) - Universidade Federal de Santa Maria, Santa Maria, 2008. |
dc.identifier.uri.fl_str_mv |
http://repositorio.ufsm.br/handle/1/4396 |
identifier_str_mv |
BORGES, Lysandro Pinto. Effects of diphenyl diselenide administration on liver damage induced by 2-nitropropane, cadmium and carbon tetrachloride. 2008. 126 f. Tese (Doutorado em Bioquímica) - Universidade Federal de Santa Maria, Santa Maria, 2008. |
url |
http://repositorio.ufsm.br/handle/1/4396 |
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Universidade Federal de Santa Maria |
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Programa de Pós-Graduação em Ciências Biológicas: Bioquímica Toxicológica |
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repository.mail.fl_str_mv |
atendimento.sib@ufsm.br||tedebc@gmail.com |
_version_ |
1793240170335567872 |