Elsevier

The Lancet

Volume 345, Issue 8943, 21 January 1995, Pages 149-151
The Lancet

Articles
Homocysteine metabolism in pregnancies complicated by neural-tube defects

https://doi.org/10.1016/S0140-6736(95)90165-5Get rights and content

Abstract

Folic acid taken around the time of conception can prevent many neural-tube defects. Women with low-normal vitamin B12 values may also be at increased risk. We considered whether homocysteine metabolism via the enzyme methionine synthase, which requires both folate and B12, could be the critical defect in folate-related neural tube defects. Blood was obtained during pregnancies that produced 81 infants with neural-tube defects and 323 normal children. Samples were assayed for homocysteine, methylmalonic acid, plasma folate, red-cell folate, and B12. Mothers of children with neural-tube defects had significantly higher homocysteine values (8·62 [SD 2·8] μmol/L) than did B12-matched controls (7·96 [2·5] μmol/L, p=0·03). The difference was significant (p=0·004) in the lower half of the B12 distribution after adjusting for plasma folate. Our study shows that an abnormality in homocysteine metabolism, apparently related to methionine synthase, is present in many women who give birth to children with neural-tube defects. Overcoming this abnormality is likely to be the mechanism by which folic acid prevents neural-tube defects. These findings suggest that the most effective periconceptional prophylaxis to prevent neural-tube defects may require B12 as well as folic acid.

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    Biological thiols (or biothiols) such as cysteine (Cys), glutathione (GSH), and homocysteine (Hcy) play essential roles in biological systems [1–3], thus their levels are closely related with diseases including cancer, metabolic diseases, brain-related diseases, et cetera [4–8].

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