Possible altered mineral metabolism in human anencephalic fetuses

James K. Friel*, Henry Longerich, Simon E. Jackson, Chitra Pushpananthan, James R. Wright

*Corresponding author for this work

    Research output: Contribution to journalArticlepeer-review

    1 Citation (Scopus)


    Neural tube defects are congenital abnormalities caused by failure of the neural tube to close during embryogenesis. We investigated trace elements (zinc, copper, manganese, cobalt, nickel, molybdenum, cadmium), livers, pancreata, sciatic nerves, diaphragms, and kidneys collected at autopsy from 33 anencephalic fetuses and 22 control fetuses. Collections were done on the right side using a titanium scalpel, plastic forceps, and acid-washed materials. Samples were wet ashed and analyzed using inductively coupled plasma mass spectrometry. The gestational age and birth weight (mean ± SD) of anencephalic fetuses were 25.8 ± 8 weeks and 729 ± 879 g, respectively; those of control fetuses, 28 ± 8 weeks and 1340 ± 1216 g, respectively. Liver concentrations (ppm, dry weight, mean ± SEM) of Zn (1075 ± 56 vs 668 ± 75; P =. 001) increased in anencephalic fetuses, suggesting defective transport of Zn. Whether this is part of the cause of neural tube defects or a result of the disease is unclear.

    Original languageEnglish
    Pages (from-to)103-109
    Number of pages7
    JournalNutrition Research
    Issue number2
    Publication statusPublished - Feb 2005


    • Cadmium
    • Human fetus
    • Neural tube defects
    • Zinc


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