Journal
BIRTH DEFECTS RESEARCH PART A-CLINICAL AND MOLECULAR TERATOLOGY
Volume 76, Issue 4, Pages 230-236Publisher
WILEY
DOI: 10.1002/bdra.20240
Keywords
neural tube defects; maternal biomarkers; folate; methionine; homocysteine; glutathione
Categories
Funding
- NCRR NIH HHS [C06 RR016517, 1C06 RR16517-01, C06 RR016517-01, 3C06 RR16517-01S1, C06 RR016517-01S16359] Funding Source: Medline
- NICHD NIH HHS [R01 HD039054-05, R01 HD039054, 5R01 HD39054-05] Funding Source: Medline
- PHS HHS [U50/CCU613236-08] Funding Source: Medline
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BACKGROUND: Alterations in maternal folate and homocysteine metabolism are associated with neural tube defects (NTDs). The role played by specific micronutrients and metabolites in the causal pathway leading to NTDs is not fully understood. METHODS: We conducted a case-control study to investigate the association between NTDs and maternal alterations in plasma micronutrients and metabolites in two metabolic pathways: methionine remethylation and glutathione transsulfuration. Biomarkers were measured in a population-based sample of women who had NTD-affected pregnancies (n = 43) and a control group of women who had a pregnancy unaffected by a birth defect (n = 160). We compared plasma concentrations of folate, vitamin B-12, vitamin 136, methionine, S-adenosylmethionine (SAM), s-adenosylhomocysteine (SAH), adenosine, homocysteine, cysteine, and reduced and oxidized glutathione between cases and controls after adjusting for lifestyle and sociodemographic factors. RESULTS: Women with NTD-affected pregnancies had significantly higher plasma concentrations of SAH (29.12 vs. 23.13 nmol/liter, P = .0011), adenosine (0.323 vs. 0.255 mu mol/liter; P = .0269), homocysteine (9.40 vs. 7.56 mu mol/liter; P < .001), and oxidized glutathione (0.379 vs. 0.262 mu mol/liter; P = .0001), but lower plasma SAM concentrations (78.99 vs. 83.16 nmol/liter; P = .0172) than controls. This metabolic profile is consistent with reduced methylation capacity and increased oxidative stress in women with affected pregnancies. CONCLUSIONS: Increased maternal oxidative stress and decreased methylation capacity may contribute to the occurrence of NTDs. Further analysis of relevant genetic and environmental factors is required to define the basis for these observed alterations. Birth Defects Research (Part A) 76:230-236, 2006. (c) 2006 Wiley-Liss, Inc.
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