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dc.creatorSTERPONE,SILVIA
dc.creatorCORNETTA,TOMMASO
dc.creatorANGIONI,ADRIANO
dc.creatorFISCARELLI,ERSILIA
dc.creatorLUCIDI,VINCENZINA
dc.creatorTESTA,ANTONELLA
dc.creatorCOZZI,RENATA
dc.date2009-01-01
dc.date.accessioned2019-05-02T21:21:52Z
dc.date.available2019-05-02T21:21:52Z
dc.identifierhttps://scielo.conicyt.cl/scielo.php?script=sci_arttext&pid=S0716-97602009000400009
dc.identifier.urihttp://revistaschilenas.uchile.cl/handle/2250/81990
dc.descriptionCystic Fibrosis (CF) is an autosomal recessive multisystemic disorder showing a highly heterogeneous phenotype, even among siblings carrying identical CFTR mutations. Moreover, oxidative stress is of central importance in the pathogenesis of cystic fibrosis. The present study seeks to value the presence of oxidative damage in CF patients and the possible modifier effect of repair and glutathione-S-transferase genes. We analysed the presence of DNA damage in leukocytes of 63 CF patients at an Italian CF centre and 63 controls, through the alkaline Comet assay to detect DNA strand breaks. Furthermore, controls and 93 CF subjects were genotyped for 5 genes by RFLP-PCR (XRCC1,0GG1,GSTP1) and PCR assay (GSTM1, GSTT1). No difference in Comet assay values was observed comparing controls to CF patients, although CF subjects showed slightly higher mean values. The crude Odds-Ratio (OR) was higher than one for XRCC1 and GSTP1 genotypes and liver status and for XRCC1 and OGG1 genotypes and pancreatic insufficiency, but in all cases the p-values were not significant. In this case-control study, neither DNA damage ñor gene polymorphisms seem to influence CF manifestation.
dc.formattext/html
dc.languageen
dc.publisherSociedad de Biología de Chile
dc.relation10.4067/S0716-97602009000400009
dc.rightsinfo:eu-repo/semantics/openAccess
dc.sourceBiological Research v.42 n.4 2009
dc.subjectComet assay
dc.subjectcystic fibrosis
dc.subjectDNA damage
dc.subjectgenetic polymorphisms
dc.subjectmodifier genes
dc.titleDNA damage and related modifier genes in Italian Cystic fibrosis patients


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