Folic acid supplementation during early hepatocarcinogenesis: cellular and molecular effects

Detalhes bibliográficos
Autor(a) principal: Andrade Chagas, Carlos Eduardo
Data de Publicação: 2011
Outros Autores: Bassoli, Bruna Kempfer, Soares de Souza, Camila Alexandre, Deminice, Rafael, Jordao Junior, Alceu Afonso, Paiva, Sergio Alberto Rupp de [UNESP], Zaidan Dagli, Maria Lucia, Ong, Thomas Prates, Moreno, Fernando Salvador
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Institucional da UNESP
Texto Completo: http://dx.doi.org/10.1002/ijc.25886
http://hdl.handle.net/11449/11386
Resumo: Folic acid (FA) supplementation during carcinogenesis is controversial. Considering the impact of liver cancer as a public health problem and mandatory FA fortification in several countries, the role of FA supplementation in hepatocarcinogenesis should be elucidated. We evaluated FA supplementation during early hepatocarcinogenesis. Rats received daily 0.08 mg (FA8 group) or 0.16 mg (FA16 group) of FA/100 g body weight or water (CO group, controls). After a 2-week treatment, animals were subjected to the "resistant hepatocyte" model of hepatocarcinogenesis (initiation with diethylnitrosamine, selection/promotion with 2-acetylaminofluorene and partial hepatectomy) and euthanized after 8 weeks of treatment. Compared to the CO group, the FA16 group presented: reduced (p < 0.05) number of persistent and increased (p < 0.05) number of remodeling glutathione S-transferase (GST-P) positive preneoplastic lesions (PNL); reduced (p < 0.05) cell proliferation in persistent GST-P positive PNL; decreased (p < 0.05) hepatic DNA damage; and a tendency (p < 0.10) for decreased c-myc expression in microdissected PNL. Regarding all these parameters, no differences (p > 0.05) were observed between CO and FA8 groups. FA-treated groups presented increased hepatic levels of S-adenosylmethionine but only FA16 group presented increased S-adenosylmethionine/S-adenosylhomocysteine ratio. No differences (p > 0.05) were observed between experimental groups regarding apoptosis in persistent and remodeling GST-P positive PNL, and global DNA methylation pattern in microdissected PNL. Altogether, the FA16 group, but not the FA8 group, presented chemopreventive activity. Reversion of PNL phenotype and inhibition of DNA damage and of c-myc expression represent relevant FA cellular and molecular effects.
id UNSP_b3f533f9f1d98d456a5755956a5f7418
oai_identifier_str oai:repositorio.unesp.br:11449/11386
network_acronym_str UNSP
network_name_str Repositório Institucional da UNESP
repository_id_str 2946
spelling Folic acid supplementation during early hepatocarcinogenesis: cellular and molecular effectsfolic acid supplementationhepatocarcinogenesischemopreventionpreneoplastic lesionsFolic acid (FA) supplementation during carcinogenesis is controversial. Considering the impact of liver cancer as a public health problem and mandatory FA fortification in several countries, the role of FA supplementation in hepatocarcinogenesis should be elucidated. We evaluated FA supplementation during early hepatocarcinogenesis. Rats received daily 0.08 mg (FA8 group) or 0.16 mg (FA16 group) of FA/100 g body weight or water (CO group, controls). After a 2-week treatment, animals were subjected to the "resistant hepatocyte" model of hepatocarcinogenesis (initiation with diethylnitrosamine, selection/promotion with 2-acetylaminofluorene and partial hepatectomy) and euthanized after 8 weeks of treatment. Compared to the CO group, the FA16 group presented: reduced (p < 0.05) number of persistent and increased (p < 0.05) number of remodeling glutathione S-transferase (GST-P) positive preneoplastic lesions (PNL); reduced (p < 0.05) cell proliferation in persistent GST-P positive PNL; decreased (p < 0.05) hepatic DNA damage; and a tendency (p < 0.10) for decreased c-myc expression in microdissected PNL. Regarding all these parameters, no differences (p > 0.05) were observed between CO and FA8 groups. FA-treated groups presented increased hepatic levels of S-adenosylmethionine but only FA16 group presented increased S-adenosylmethionine/S-adenosylhomocysteine ratio. No differences (p > 0.05) were observed between experimental groups regarding apoptosis in persistent and remodeling GST-P positive PNL, and global DNA methylation pattern in microdissected PNL. Altogether, the FA16 group, but not the FA8 group, presented chemopreventive activity. Reversion of PNL phenotype and inhibition of DNA damage and of c-myc expression represent relevant FA cellular and molecular effects.Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Univ São Paulo, Fac Pharmaceut Sci, Dept Food & Expt Nutr, Lab Diet Nutr & Canc, São Paulo, BrazilUniv São Paulo, Fac Med Ribeirao Preto, Dept Med, Lab Nutr & Metab,Div Nutrol, São Paulo, BrazilSão Paulo State Univ, Fac Med, Dept Med, Botucatu, SP, BrazilUniv São Paulo, Fac Vet Med & Zootechny, Dept Pathol, Expt Oncol Lab, São Paulo, BrazilSão Paulo State Univ, Fac Med, Dept Med, Botucatu, SP, BrazilFAPESP: 06/60726-1Wiley-BlackwellUniversidade de São Paulo (USP)Universidade Estadual Paulista (Unesp)Andrade Chagas, Carlos EduardoBassoli, Bruna KempferSoares de Souza, Camila AlexandreDeminice, RafaelJordao Junior, Alceu AfonsoPaiva, Sergio Alberto Rupp de [UNESP]Zaidan Dagli, Maria LuciaOng, Thomas PratesMoreno, Fernando Salvador2014-05-20T13:33:18Z2014-05-20T13:33:18Z2011-11-01info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/article2073-2082http://dx.doi.org/10.1002/ijc.25886International Journal of Cancer. Malden: Wiley-blackwell, v. 129, n. 9, p. 2073-2082, 2011.0020-7136http://hdl.handle.net/11449/1138610.1002/ijc.25886WOS:000295230500003Web of Sciencereponame:Repositório Institucional da UNESPinstname:Universidade Estadual Paulista (UNESP)instacron:UNESPengInternational Journal of Cancer7.3603,152info:eu-repo/semantics/openAccess2021-10-23T11:33:44Zoai:repositorio.unesp.br:11449/11386Repositório InstitucionalPUBhttp://repositorio.unesp.br/oai/requestopendoar:29462021-10-23T11:33:44Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP)false
dc.title.none.fl_str_mv Folic acid supplementation during early hepatocarcinogenesis: cellular and molecular effects
title Folic acid supplementation during early hepatocarcinogenesis: cellular and molecular effects
spellingShingle Folic acid supplementation during early hepatocarcinogenesis: cellular and molecular effects
Andrade Chagas, Carlos Eduardo
folic acid supplementation
hepatocarcinogenesis
chemoprevention
preneoplastic lesions
title_short Folic acid supplementation during early hepatocarcinogenesis: cellular and molecular effects
title_full Folic acid supplementation during early hepatocarcinogenesis: cellular and molecular effects
title_fullStr Folic acid supplementation during early hepatocarcinogenesis: cellular and molecular effects
title_full_unstemmed Folic acid supplementation during early hepatocarcinogenesis: cellular and molecular effects
title_sort Folic acid supplementation during early hepatocarcinogenesis: cellular and molecular effects
author Andrade Chagas, Carlos Eduardo
author_facet Andrade Chagas, Carlos Eduardo
Bassoli, Bruna Kempfer
Soares de Souza, Camila Alexandre
Deminice, Rafael
Jordao Junior, Alceu Afonso
Paiva, Sergio Alberto Rupp de [UNESP]
Zaidan Dagli, Maria Lucia
Ong, Thomas Prates
Moreno, Fernando Salvador
author_role author
author2 Bassoli, Bruna Kempfer
Soares de Souza, Camila Alexandre
Deminice, Rafael
Jordao Junior, Alceu Afonso
Paiva, Sergio Alberto Rupp de [UNESP]
Zaidan Dagli, Maria Lucia
Ong, Thomas Prates
Moreno, Fernando Salvador
author2_role author
author
author
author
author
author
author
author
dc.contributor.none.fl_str_mv Universidade de São Paulo (USP)
Universidade Estadual Paulista (Unesp)
dc.contributor.author.fl_str_mv Andrade Chagas, Carlos Eduardo
Bassoli, Bruna Kempfer
Soares de Souza, Camila Alexandre
Deminice, Rafael
Jordao Junior, Alceu Afonso
Paiva, Sergio Alberto Rupp de [UNESP]
Zaidan Dagli, Maria Lucia
Ong, Thomas Prates
Moreno, Fernando Salvador
dc.subject.por.fl_str_mv folic acid supplementation
hepatocarcinogenesis
chemoprevention
preneoplastic lesions
topic folic acid supplementation
hepatocarcinogenesis
chemoprevention
preneoplastic lesions
description Folic acid (FA) supplementation during carcinogenesis is controversial. Considering the impact of liver cancer as a public health problem and mandatory FA fortification in several countries, the role of FA supplementation in hepatocarcinogenesis should be elucidated. We evaluated FA supplementation during early hepatocarcinogenesis. Rats received daily 0.08 mg (FA8 group) or 0.16 mg (FA16 group) of FA/100 g body weight or water (CO group, controls). After a 2-week treatment, animals were subjected to the "resistant hepatocyte" model of hepatocarcinogenesis (initiation with diethylnitrosamine, selection/promotion with 2-acetylaminofluorene and partial hepatectomy) and euthanized after 8 weeks of treatment. Compared to the CO group, the FA16 group presented: reduced (p < 0.05) number of persistent and increased (p < 0.05) number of remodeling glutathione S-transferase (GST-P) positive preneoplastic lesions (PNL); reduced (p < 0.05) cell proliferation in persistent GST-P positive PNL; decreased (p < 0.05) hepatic DNA damage; and a tendency (p < 0.10) for decreased c-myc expression in microdissected PNL. Regarding all these parameters, no differences (p > 0.05) were observed between CO and FA8 groups. FA-treated groups presented increased hepatic levels of S-adenosylmethionine but only FA16 group presented increased S-adenosylmethionine/S-adenosylhomocysteine ratio. No differences (p > 0.05) were observed between experimental groups regarding apoptosis in persistent and remodeling GST-P positive PNL, and global DNA methylation pattern in microdissected PNL. Altogether, the FA16 group, but not the FA8 group, presented chemopreventive activity. Reversion of PNL phenotype and inhibition of DNA damage and of c-myc expression represent relevant FA cellular and molecular effects.
publishDate 2011
dc.date.none.fl_str_mv 2011-11-01
2014-05-20T13:33:18Z
2014-05-20T13:33:18Z
dc.type.status.fl_str_mv info:eu-repo/semantics/publishedVersion
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
format article
status_str publishedVersion
dc.identifier.uri.fl_str_mv http://dx.doi.org/10.1002/ijc.25886
International Journal of Cancer. Malden: Wiley-blackwell, v. 129, n. 9, p. 2073-2082, 2011.
0020-7136
http://hdl.handle.net/11449/11386
10.1002/ijc.25886
WOS:000295230500003
url http://dx.doi.org/10.1002/ijc.25886
http://hdl.handle.net/11449/11386
identifier_str_mv International Journal of Cancer. Malden: Wiley-blackwell, v. 129, n. 9, p. 2073-2082, 2011.
0020-7136
10.1002/ijc.25886
WOS:000295230500003
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv International Journal of Cancer
7.360
3,152
dc.rights.driver.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv 2073-2082
dc.publisher.none.fl_str_mv Wiley-Blackwell
publisher.none.fl_str_mv Wiley-Blackwell
dc.source.none.fl_str_mv Web of Science
reponame:Repositório Institucional da UNESP
instname:Universidade Estadual Paulista (UNESP)
instacron:UNESP
instname_str Universidade Estadual Paulista (UNESP)
instacron_str UNESP
institution UNESP
reponame_str Repositório Institucional da UNESP
collection Repositório Institucional da UNESP
repository.name.fl_str_mv Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP)
repository.mail.fl_str_mv
_version_ 1799964472555601920