Oxidative DNA damage in diabetic and mild gestational hyperglycemic pregnant women

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dc.contributor.authorGelaleti, Rafael Bottaro [UNESP]
dc.contributor.authorDamasceno, Debora Cristina [UNESP]
dc.contributor.authorOrtiz Lima, Paula Helena
dc.contributor.authorFavero Salvadori, Daisy Maria [UNESP]
dc.contributor.authorParanhos Calderon, Iracema de Mattos [UNESP]
dc.contributor.authorPeracoli, José Carlos [UNESP]
dc.contributor.authorCunha Rudge, Marilza Vieira [UNESP]
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.contributor.institutionInstituto Dante Pazzanese de Cardiologia
dc.date.accessioned2015-10-21T13:09:01Z
dc.date.available2015-10-21T13:09:01Z
dc.date.issued2015-01-15
dc.description.abstractBackground: Pregnant women with mild gestational hyperglycemia present high risk for hypertension, obesity and hyperglycemia, and appeared to reproduce the model of metabolic syndrome in pregnancy, with hyperinsulinemia and insulin resistance. Our clinical studies showed that mild gestational hyperglycemia or gestational diabetes are related to similar adverse maternal and perinatal outcomes. Hyperglycemia and other factors associated with diabetes generate reactive oxygen species that increase DNA damage levels. The aim of this study was to evaluate oxidative DNA damage in lymphocytes of pregnant women with diabetes or mild gestational hyperglycemia.Methods: The study included 111 pregnant women distributed into three groups based on oral glucose tolerance test (OGTT) and glycemic profiles (GP), as follows: Normal OGTT and GP (control group); Normal OGTT and abnormal GP (mild gestational hyperglycemia group); Abnormal OGTT and GP (diabetic group). Maternal blood samples (5-10 mL) were collected and processed for determination of oxidative DNA damage by the comet assay, using Fpg and Endo III enzymes. Urine samples were also collected for determination of 8-OHdG concentrations by ELISA.Results: Subjects in the diabetes group presented increased amount of oxidized purines, while mild gestational hyperglycemia women presented with increased oxidized pyrimidines, compared to the control group.Conclusion: Gestational, overt diabetes and mild gestational hyperglycemia, were all related to increased oxidative DNA damage. Diabetic pregnant women showed increased level of oxidative DNA damage, perhaps mainly due to hyperglycemia. On the other hand, oxidative DNA damage detected in women with mild gestational hyperglycemia might be associated with repercussions from obesity, hypertension and/or insulin resistance. Interestingly, the type of DNA base affected seemed to be dependent on the glycemic profile or oxidative stress.en
dc.description.affiliationInstituto Dante Pazzanese de Cardiologia, São Paulo, SP, Brazil
dc.description.affiliationUnespUniversidade Estadual Paulista, Departamento de Ginecologia e Obstetrícia, Faculdade de Medicina de Botucatu, UNESP, Distrito de Rubião Júnior s/n, CEP. 18618.000, Botucatu, São Paulo, Brazil
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorshipIdFAPESP: 2008/06642-6
dc.format.extent1-7
dc.identifierhttp://www.dmsjournal.com/content/7/1/1
dc.identifier.citationDiabetology & Metabolic Syndrome. London: Biomed Central Ltd, v. 7, p. 7, 2015.
dc.identifier.doi10.1186/1758-5996-7-1
dc.identifier.fileWOS000349476400001.pdf
dc.identifier.issn1758-5996
dc.identifier.lattes5051118752980903
dc.identifier.lattes8499437381595614
dc.identifier.lattes6758680388835078
dc.identifier.urihttp://hdl.handle.net/11449/128327
dc.identifier.wosWOS:000349476400001
dc.language.isoeng
dc.publisherBiomed Central Ltd
dc.relation.ispartofDiabetology & Metabolic Syndrome
dc.relation.ispartofjcr2.413
dc.relation.ispartofsjr0,943
dc.rights.accessRightsAcesso aberto
dc.sourceWeb of Science
dc.subjectDiabetesen
dc.subjectPregnancyen
dc.subjectMild gestational hyperglycemiaen
dc.subjectGenotoxicityen
dc.subjectOxidative DNA damageen
dc.titleOxidative DNA damage in diabetic and mild gestational hyperglycemic pregnant womenen
dc.typeArtigo
dcterms.rightsHolderBiomed Central Ltd
unesp.author.lattes5051118752980903
unesp.author.lattes8499437381595614
unesp.author.lattes6758680388835078
unesp.author.orcid0000-0002-7003-9643[2]
unesp.author.orcid0000-0002-6098-9899[1]
unesp.author.orcid0000-0003-4761-4336[5]
unesp.author.orcid0000-0001-9323-3134[4]
unesp.author.orcid0000-0002-9227-832X[7]
unesp.campusUniversidade Estadual Paulista (Unesp), Faculdade de Medicina, Botucatupt

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