Utilize este identificador para referenciar este registo: http://hdl.handle.net/10451/28678
Registo completo
Campo DCValorIdioma
degois.publication.firstPage179pt_PT
degois.publication.lastPage183pt_PT
degois.publication.titleMutagenesispt_PT
dc.relation.publisherversionhttps://academic.oup.com/mutage/article-abstract/1/3/179/1150225/Genetic-toxicology-of-flavonoids-the-role-of?redirectedFrom=fulltextpt_PT
dc.contributor.authorRueff, José-
dc.contributor.authorLaires, António-
dc.contributor.authorBorba, Helena-
dc.contributor.authorChaveca, Teresa-
dc.contributor.authorGomes, Maria Inácia-
dc.contributor.authorHapern, Manuel-
dc.date.accessioned2017-08-11T15:08:27Z-
dc.date.available2017-08-11T15:08:27Z-
dc.date.issued1986-
dc.identifier.citationMutagenesis. 1986;1(3):179-183pt_PT
dc.identifier.issn0267-8357-
dc.identifier.urihttp://hdl.handle.net/10451/28678-
dc.description.abstractGlycosides of flavonols such as quercetin, are found in the edible portions of most food vegetables. Flavonols present in plants as glycosides can be freed during fermentation. We have compared the DNA-damaging activity of quercetin, rutin (3-o-rutinoside of quercetin) and a fermented flavonoid-containing beverage, red wine, for different genetic end-points under different metabolic conditions. The genotoxicity of quercetin, rutin and commercial red wine has been studied for the induction of: (i) reverse mutation in the Ames assay; (ii) SOS functions in the SOS Chromotest; (iii) sister-chro-matid exchanges (SCEs) in human lymphocytes. While in the Ames assay the mutagenicity of quercetin is enhanced by the presence of rat liver microsomal enzymes (S9) or the respective cytosolic fraction (S100), genotoxicity is reduced when the induction of SOS responses is assessed using the SOS Chromotest. Similarly, the induction of SCEs is lowered when testing in the presence of liver enzymes. Rutin has no activity whatsoever. Detection of activity of red wine in the three assays is not dependent upon hydrolysis by glycosidases and its content of quercetin accounts almost entirely for the levels of genotoxicity detected. The results suggest that the putative genotoxic metabolites of quercetin vary for different genetic end-points considered and that the metabolic fate of flavonoids might partly account for the conflicting data about their genotoxicity in vivo and carcinogenic activity.pt_PT
dc.description.sponsorshipThe advice of Professor M. Hofnung during this study is gratefully acknowledged. Our appreciation is extended to Dr P. Quiilardet for his invaluable suggestions. This work was supported in part by the National Institute of Scientific Investigation (INIC) through research contract no. 85/CSA/16.pt_PT
dc.language.isoengpt_PT
dc.rightsrestrictedAccesspt_PT
dc.titleGenetic toxicology of flavonoids : the role of metabolic conditions in the induction of reverse mutation, SOS functions and sister-chromatid exchangespt_PT
dc.typearticlept_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.peerreviewedyespt_PT
degois.publication.volume1pt_PT
dc.identifier.doihttps://doi.org/10.1093/mutage/1.3.179pt_PT
Aparece nas colecções:FF - Separatas (Biblioteca)

Ficheiros deste registo:
Ficheiro Descrição TamanhoFormato 
9653.pdf536,57 kBAdobe PDFVer/Abrir    Acesso Restrito. Solicitar cópia ao autor!


FacebookTwitterDeliciousLinkedInDiggGoogle BookmarksMySpace
Formato BibTex MendeleyEndnote Degois 

Todos os registos no repositório estão protegidos por leis de copyright, com todos os direitos reservados.