dc.contributorUniv Texas Med Branch
dc.contributorUniversidade Estadual Paulista (Unesp)
dc.creatorMenon, Ramkumar
dc.creatorPolettini, Jossimara [UNESP]
dc.creatorSyed, Tariq Ali
dc.creatorSaade, George R.
dc.creatorBoldogh, Istvan
dc.date2014-12-03T13:10:36Z
dc.date2014-12-03T13:10:36Z
dc.date2014-07-01
dc.date.accessioned2023-09-09T09:57:00Z
dc.date.available2023-09-09T09:57:00Z
dc.identifierhttp://dx.doi.org/10.1111/aji.12220
dc.identifierAmerican Journal Of Reproductive Immunology. Hoboken: Wiley-blackwell, v. 72, n. 1, p. 75-84, 2014.
dc.identifier1046-7408
dc.identifierhttp://hdl.handle.net/11449/112295
dc.identifier10.1111/aji.12220
dc.identifierWOS:000337752700009
dc.identifier.urihttps://repositorioslatinoamericanos.uchile.cl/handle/2250/8761926
dc.descriptionProblem The most common DNA lesion generated by oxidative stress (OS) is 7, 8-dihydro-8-oxoguanine (8-oxoG) whose excision repair is performed by 8-oxoguanine glycosylase (OGG1). We investigated OGG1 expression changes in fetal membranes from spontaneous preterm birth (PTB) and preterm premature rupture of the membranes (pPROM) and its changes in vitro in normal fetal membranes exposed to OS inducer water-soluble cigarette smoke extract (CSE). Method of study DNA damage was determined in amnion cells treated with CSE by comet and FLARE assays. OGG1 mRNA expression and localization in fetal membranes from clinical specimens and in normal term membranes exposed to CSE were examined by QRT-PCR and by immunohistochemistry. Results DNA strand and base damage was seen in amnion cells exposed to CSE. OGG1 expression was 2.5-fold higher in PTB samples compared with pPROM (P=0.045). No significant difference was seen between term and pPROM or PTB and term. CSE treatment showed a nonsignificant decrease in OGG1. OGG1 was localized to both amnion and chorion with less intense staining in pPROM and CSE-treated membranes. Conclusion Increased OS-induced DNA damage predominated by 8-oxoG is likely to persist in fetal cells due to reduced availability of base excision repair enzyme OGG1. This can likely lead to fetal cell senescence associated with some adverse pregnancy outcome.
dc.descriptionDepartment of Obstetrics and Gynecology, The University of Texas Medical Branch
dc.descriptionUniv Texas Med Branch, Dept Obstet & Gynecol, Div Maternal Fetal Med Perinatal Res, Galveston, TX 77555 USA
dc.descriptionUNESP Univ Estadual Paulista, Botucatu Med Sch, Dept Pathol, Sao Paulo, Brazil
dc.descriptionUniv Texas Med Branch, Dept Microbiol & Immunol, Galveston, TX 77555 USA
dc.descriptionUNESP Univ Estadual Paulista, Botucatu Med Sch, Dept Pathol, Sao Paulo, Brazil
dc.format75-84
dc.languageeng
dc.publisherWiley-Blackwell
dc.relationAmerican Journal of Reproductive Immunology
dc.relation2.745
dc.relation1,210
dc.rightsAcesso restrito
dc.sourceWeb of Science
dc.subjectBase excision repair
dc.subjectDNA damage
dc.subjectDNA repair
dc.subjectoxidative stress
dc.subjectpreterm premature rupture of the membranes
dc.subjectprematurity
dc.titleExpression of 8-oxoguanine Glycosylase in Human Fetal Membranes
dc.typeArtigo


Este ítem pertenece a la siguiente institución