Chronic ethanol intake promotes double gluthatione S-transferase transforming growth factor-alpha-positive hepatocellular lesions in male Wistar rats

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dc.contributor.authorPires, Paulo Wagner [UNESP]
dc.contributor.authorFurtado, Kelly Silva [UNESP]
dc.contributor.authorJustullin, Luis Antonio [UNESP]
dc.contributor.authorRodrigues, Maria Aparecida Marchesan [UNESP]
dc.contributor.authorFelisbino, Sergio Luis [UNESP]
dc.contributor.authorBarbisan, Luis Fernando [UNESP]
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.contributor.institutionUniversidade Estadual de Campinas (UNICAMP)
dc.date.accessioned2014-05-20T13:37:31Z
dc.date.available2014-05-20T13:37:31Z
dc.date.issued2008-02-01
dc.description.abstractThe chronic ethanol intake influence on the gluthatione S-transferase (GST-P) and transforming growth factor alpha (TGF-alpha) expression in remodeling/persistent preneoplastic lesions (PNLs) was evaluated in the resistant hepatocyte model. Male Wistar rats were allocated into five groups: G1, non-treated, fed water and chow ad libitum; G2, non-treated and pair-fed chow (restricted to match that of G3 group) and a maltodextrin (MD) solution in tap water (matched ethanol-derived calories); G3, fed 5% ethanol in drinking water and chow ad libitum; G4, diethylnitrosamine (DEN, 200 mg/kg, body weight) plus 200 parts per million of 2-acetylaminofluorene (2-AAF) for 3 weeks and pair-fed chow (restricted to match that of G5 group) and an MD solution in tap water (matched ethanol-derived calories); G5, DEN/2-AAF treatment, fed ethanol 5% and chow ad libitum. All animals were subjected to 70% partial hepatectomy at week 3 and sacrificed at weeks 12 or 22, respectively. Liver samples were collected for histological analysis or immunohistochemical expression of GST-P, TGF-alpha and proliferating cell nuclear antigen or zymography for matrix metalloproteinases-2 and -9. At the end of ethanol treatment, there was a significant increase in the percentage of liver area occupied by persistent GST-P-positive PNLs, the number of TGF-alpha-positive PNLs and the development of liver tumors in ethanol-fed and DEN/2-AAF-treated groups (G5 versus G4, P < 0.001). In addition, ethanol feeding led to a significant increase in cell proliferation mainly in remodeling and persistent PNLs with immunoreactivity for TGF-alpha at week 22 (P < 0.001). Gelatinase activities were not altered by ethanol treatment. The results demonstrated that ethanol enhances the selective growth of PNL with double expression of TGF-alpha and GST-P markers.en
dc.description.affiliationSão Paulo State Univ, UNESP, Inst Biosci, Dept Morphol, BR-18618000 Botucatu, SP, Brazil
dc.description.affiliationUniv Estadual Campinas, Inst Biol, Dept Cell Biol, BR-13083950 Campinas, SP, Brazil
dc.description.affiliationSão Paulo State Univ, UNESP, Sch Med, Dept Pathol, BR-18618000 Botucatu, SP, Brazil
dc.description.affiliationUnespSão Paulo State Univ, UNESP, Inst Biosci, Dept Morphol, BR-18618000 Botucatu, SP, Brazil
dc.description.affiliationUnespSão Paulo State Univ, UNESP, Sch Med, Dept Pathol, BR-18618000 Botucatu, SP, Brazil
dc.format.extent221-228
dc.identifierhttp://dx.doi.org/10.1111/j.1349-7006.2007.00677.x
dc.identifier.citationCancer Science. Oxford: Blackwell Publishing, v. 99, n. 2, p. 221-228, 2008.
dc.identifier.doi10.1111/j.1349-7006.2007.00677.x
dc.identifier.issn1347-9032
dc.identifier.lattes7263490918934874
dc.identifier.lattes3278528112652257
dc.identifier.urihttp://hdl.handle.net/11449/12998
dc.identifier.wosWOS:000252966800006
dc.language.isoeng
dc.publisherBlackwell Publishing
dc.relation.ispartofCancer Science
dc.relation.ispartofsjr1,744
dc.rights.accessRightsAcesso aberto
dc.sourceWeb of Science
dc.titleChronic ethanol intake promotes double gluthatione S-transferase transforming growth factor-alpha-positive hepatocellular lesions in male Wistar ratsen
dc.typeArtigo
dcterms.licensehttp://olabout.wiley.com/WileyCDA/Section/id-406071.html
dcterms.rightsHolderBlackwell Publishing
unesp.author.lattes7263490918934874
unesp.author.lattes3278528112652257
unesp.author.orcid0000-0001-5972-4554[1]
unesp.campusUniversidade Estadual Paulista (Unesp), Instituto de Biociências, Botucatupt
unesp.campusUniversidade Estadual Paulista (Unesp), Faculdade de Medicina, Botucatupt

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