Hyperzincemia in anencephaly and spina bifida: a clue to the pathogenesis of neural tube defects?
Zinc is essential for normal embryogenesis and may have particular importance for closure of the human neural tube. Compared to 258 controls, we found increased zinc content in umbilical cord serum in eight of nine newborn anencephalics (p less than 0.02) and three infants with spina bifida (p less than 0.001). Increased zinc levels were bound to serum albumin or alpha-2-macroglobulin (alpha 2M) in infants with neural tube defects (NTD). In NTD-mothers, total serum zinc was similar to controls, but there was a shift in the distribution of zinc from alpha 2M to albumin. Fetal hyperzincemia and elevated maternal albumin-bound zinc suggest that the NTD-fetus receives but does not use zinc normally.
D000328:Adult; D000757:Anencephaly / Q000097:blood*; D001798:Blood Proteins / Q000378:metabolism; D005260:Female; D005312:Fetal Blood / Q000378:metabolism; D006801:Humans; D007231:Infant, Newborn; D008297:Male; D008431:Maternal-Fetal Exchange; D009436:Neural Tube Defects / Q000097:blood* / Q000209:etiology; D011247:Pregnancy; D011296:Prenatal Diagnosis; D016136:Spina Bifida Occulta / Q000097:blood*; D015032:Zinc / Q000097:blood*
D001798:Blood Proteins; D015032:Zinc