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Please use this identifier to cite or link to this item: http://repositorio.insp.mx:8080/jspui/handle/20.500.12096/8019
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dc.coverage.spatialnacional
dc.creatorAmarasiriwardena, Chitra
dc.date.accessioned2022-02-16T04:24:28Z-
dc.date.available2022-02-16T04:24:28Z-
dc.date.issued2019
dc.identifier.urisicabi.insp.mx:2019-None
dc.identifier.urihttps://www.sciencedirect.com/science/article/pii/S0160412018322086?via%3Dihub
dc.identifier.urihttps://www.doi.org/10.1016/j.envint.2019.02.029
dc.identifier.urihttp://repositorio.insp.mx:8080/jspui/handle/20.500.12096/8019-
dc.description.abstractINTRODUCTION Manganese (Mn) is an essential nutrient but also a toxicant at high exposures, when it can induce oxidative stress (OS). Mn uptake is inversely correlated with iron status, therefore anemic individuals may be more susceptible to Mn overload induced-OS, which can manifest as changes in mitochondrial DNA copy number (mtDNA CN). Our s were to: 1) determine stage-specific associations of prenatal Mn exposure with cord blood MtDNA CN; and 2) investigate effect modification by maternal anemia, ferritin, and mean corpuscular volume (MCV). MATERIALS AND METHODS: We measured whole blood Mn, hemoglobin, serum ferritin, and MCV in the 2nd and 3rd trimester, in maternal blood at birth, and in cord blood from a prospective birth cohort in Mexico City, Mexico (n = 485). We then extracted DNA from cord blood leukocytes to determine mtDNA CN. We used robust regression to measure associations between Mn and mtDNA CN at each trimester and at birth. Anemia (hemoglobin ≤11 g/dL), iron deficiency (ferritin ≤15 ng/mL) and MCV (stratified at median), were examined as effect modifiers. RESULTS: Mn levels increased throughout pregnancy, and Mn was inversely correlated with ferritin. We observed a positive association between Mn in the 3rd trimester and Mn in cord blood and mtDNA CN (β = 0.04-0.05; 95% CI = 0.01, 0.08). Anemia significantly modified the association between mtDNA CN and Mn in the 2nd trimester. We found a positive association between 2nd trimester Mn and mtDNA CN in mothers with normal hemoglobin, and a negative association in those with low hemoglobin. (βhigh = 0.06; 95% CI = 0.01, 0.11; p = 0.01 and βlow = -0.06; 95% CI = 0.03, -0.13; p = 0.06). No associations were detected between anemia, iron deficiency and MCV and mtDNA CN. CONCLUSIONS: Maternal blood Mn in the 3rd trimester and in cord blood was positively associated with mtDNA CN, suggesting that higher late pregnancy prenatal Mn exposures can impact newborn mitochondria by promoting OS. Furthermore, 2nd trimester Mn was positively associated with mtDNA in non-anemic mother-child pairs but inversely associated in anemic individuals, indicating potential interactions between Mn and chronic anemia.
dc.formatpdf
dc.languagespa
dc.publisherESPM INSP
dc.rightsinfo:eu-repo/semantics/openAccess
dc.rightshttp://creativecommons.org/licenses/by-nc-nd/4.0
dc.subjectAdultAnemiablood,DNA Copy Number VariationsDNA, Mitochondrialanalysis,Environmental PollutantsbloodFemaleFetal BloodchemistryHumansInfant, NewbornMaleManganesebloodMaternal-Fetal ExchangeMexicoMothersPregnancyPregnancy Trimester, ThirdYoung Adult,SD
dc.titlePrenatal manganese and cord blood mitochondrial DNA copy number: Effect modification by maternal anemic status
dc.typeinfo:eu-repo/semantics/article
dc.subject.ctiinfo:eu-repo/classification/cti/3
dc.creator.orcidorcid/0000-0002-7031-8140;Amarasiriwardena, Chitra
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