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Serum zinc, selenium, copper, and lead levels in women with second-trimester induced abortion resulting from neural tube defects

A preliminary study

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Abstract

Neural tube defects are important causes of infant mortality and childhood morbidity. We investigated the relationship between zinc, selenium, copper, and lead concentrations and neural-tube-defect occurrence in women with a second-trimester termination due to fetal-neural-tube defects (NTDs) in this case-control study. Fourteen pregnant women whose pregnancies were terminated as a result of second-trimester ultrasonographic diagnosis of neural tube defects were recruited as cases. The control group (n=14) consisted of women who were selected among age-, gravidity-, and socio-economic-state (SES)-matched women who had a normal triple-screen and targeted ultrasound during the second trimester with documented normal fetal outcome. Zinc and copper determinations were made using flame atomic absorption spectrophotometer (AAS). Graphite furnace AAS was used for Pb, and Se levels were measured with hydride generation AAS. Cases had significantly low serum zinc and selenium levels (62.48±15.9 vs 102.6±23.7 and 55.16±11.3 vs 77.4±5.5, respectively, p<0.001). Serum Cu and whole-blood Pb levels were significantly high when compared to controls. There was a negative correlation between serum zinc and selenium levels, and serum copper levels (r=−425 and −0.443, p<0.05). Our results are consistent with some previous reports. The etiology of NTDs cannot be explained with one strict etiologic mechanism. On the contrary, an interaction among environmental, genetic, and nutritional factors such as trace elements and vitamins would explain these anomalies. If folic acid supplementation is given, additional Zn supplementation should be considered for the further decrease in the recurrence and occurrence of NTDs.

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Cengiz, B., Söylemez, F., Öztürk, E. et al. Serum zinc, selenium, copper, and lead levels in women with second-trimester induced abortion resulting from neural tube defects. Biol Trace Elem Res 97, 225–235 (2004). https://doi.org/10.1385/BTER:97:3:225

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  • DOI: https://doi.org/10.1385/BTER:97:3:225

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