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Authordc.contributor.authorSignore, Caroline 
Authordc.contributor.authorAros Aránguiz, Sofía Daniela es_CL
Authordc.contributor.authorMorrow, Jason D. es_CL
Authordc.contributor.authorTroendle, James es_CL
Authordc.contributor.authorConley, Mary R. es_CL
Authordc.contributor.authorFlanigan, Elizabeth Y. es_CL
Authordc.contributor.authorCassorla Goluboff, Fernando es_CL
Authordc.contributor.authorMills, James L. es_CL
Admission datedc.date.accessioned2010-01-19T14:21:35Z
Available datedc.date.available2010-01-19T14:21:35Z
Publication datedc.date.issued2008-11
Cita de ítemdc.identifier.citationALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH, Volume: 32, Issue: 11, Pages: 1893-1898, 2008en_US
Identifierdc.identifier.issn0145-6008
Identifierdc.identifier.urihttps://repositorio.uchile.cl/handle/2250/128248
Abstractdc.description.abstractBackground: The precise pathway by which alcohol causes the characteristic features of fetal alcohol spectrum disorders is unknown. Proposed mechanisms for fetal injury from maternal alcohol use include cellular damage from oxidative stress and impaired fetal oxygenation related to maternal systemic vasoconstriction. Our objective was to compare the levels of urinary markers of oxidative stress and systemic vasoconstriction between women consuming large amounts of alcohol during pregnancy and women who did not drink alcohol during pregnancy. Methods: Pregnant women consuming ‡48 g alcohol per day (n = 29) on average and pregnant women who abstained from alcohol use (n = 39) were identified using detailed interviews and home visits. Random maternal urine specimens were collected. Urinary levels of the oxidative stress marker, 8-isoprostane F2a, and of the vasoactive prostaglandin metabolites, 2,3-dinor- 6-keto-prostaglandin F1a (a vasodilator) and 11-dehydro-thromboxane B2 (a vasoconstrictor), were measured using mass spectrometric methods. All analyte levels were corrected for urinary creatinine. Results: In crude analyses, there was no significant difference in 8-isoprostane F2a between pregnant drinkers and nondrinkers (2.16 vs. 2.08 ng ⁄mg creatinine, respectively, p = 0.87). There were no significant differences between the drinking and nondrinking groups in levels of 2, 3-dinor-6-keto-prostaglandin F1a (1.03 vs. 1.17 ng ⁄ mg creatinine, repectively, p = 0.50), 11-dehydro-thromboxane B2 (0.72 vs. 0.59 ng ⁄ mg creatinine, respectively, p = 0.21), or the ratio of vasodilatory metabolite to vasoconstrictive metabolite (1.73 vs. 2.72, respectively, p = 0.14). Adjusting for maternal age, marital status, smoking, and gestational age at sampling did not substantially alter the results. Conclusion: Our results show no difference in levels of urinary eicosanoid markers of oxidative stress and systemic vasoconstriction between pregnant women who drink heavily and pregnant women who abstain. These findings speak against a role for maternal oxidative stress or systemic vasoconstriction in the pathogenesis of alcohol damage to the fetus.en_US
Patrocinadordc.description.sponsorshipThis research was supported by the Intramural Research Program of the Eunice Kennedy Shriver National Institute of Child Health and Human Development and by National Institutes of Health grants GM15431, DK48831 and ES131 25.en_US
Lenguagedc.language.isoenen_US
Publisherdc.publisherBLACKWELL PUBLISHINGen_US
Keywordsdc.subjectAlcoholen_US
Títulodc.titleMarkers of Oxidative Stress and Systemic Vasoconstriction in Pregnant Women Drinking ‡48 g of Alcohol per Dayen_US
Document typedc.typeArtículo de revista


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