Markers of oxidative stress and systemic vasoconstriction in pregnant women drinking > or =48 g of alcohol per day.
BACKGROUND
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 > or =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 F2alpha, and of the vasoactive prostaglandin metabolites, 2,3-dinor-6-keto-prostaglandin F1alpha (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 F2alpha 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 F1alpha (1.03 vs. 1.17 ng/mg creatinine, respectively, 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.


CONCLUSIONS
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.
Signore
Caroline
C
Epidemiology Branch, Division of Epidemiology, Statistics, and Prevention Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892, USA.
Aros
Sofía
S
Morrow
Jason D
JD
Troendle
James
J
Conley
Mary R
MR
Flanigan
Elizabeth Y
EY
Cassorla
Fernando
F
Mills
James L
JL
D015121:6-Ketoprostaglandin F1 alpha / Q000031:analogs & derivatives / Q000652:urine; D000293:Adolescent; D000328:Adult; D000428:Alcohol Drinking / Q000009:adverse effects / Q000503:physiopathology*; D016022:Case-Control Studies; D002492:Central Nervous System Depressants / Q000009:adverse effects; D015331:Cohort Studies; D015237:Dinoprost / Q000031:analogs & derivatives / Q000652:urine; D015777:Eicosanoids / Q000652:urine*; D000431:Ethanol / Q000009:adverse effects; D005260:Female; D063647:Fetal Alcohol Spectrum Disorders / Q000209:etiology* / Q000503:physiopathology; D005500:Follow-Up Studies; D006801:Humans; D028421:Isoprostanes / Q000652:urine*; D018384:Oxidative Stress / Q000502:physiology*; D011247:Pregnancy; D013929:Thromboxane B2 / Q000031:analogs & derivatives / Q000652:urine; D014661:Vasoconstriction / Q000502:physiology*; D055815:Young Adult
D002492:Central Nervous System Depressants; D015777:Eicosanoids; D028421:Isoprostanes; C075750:8-epi-prostaglandin F2alpha; D000431:Ethanol; D013929:Thromboxane B2; D015121:6-Ketoprostaglandin F1 alpha; C028290:2,3-dinor-6-ketoprostaglandin F1alpha; C049235:11-dehydro-thromboxane B2; D015237:Dinoprost