Possible altered mineral metabolism in human anencephalic fetuses

• Published in: Nutrition research (New York, N.Y.) Vol. 25; no. 2; pp. 103 - 109
• Main Authors: Friel, James K., Longerich, Henry, Jackson, Simon E., Pushpananthan, Chitra, Wright, James R.
• Format: Journal Article
• Language: English
• Published: Elsevier Inc 2005
• Subjects: Cadmium; congenital abnormalities; diaphragm; dietary minerals; fetus; Human fetus; kidneys; liver; mineral metabolism; nerve tissue; Neural tube defects; pancreas; pregnancy; pregnancy complications; spina bifida; Zinc; Cadmium; Human fetus; Neural tube defects; Zinc
• ISSN: 0271-5317; 1879-0739
• DOI: 10.1016/j.nutres.2004.10.007

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.