{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,6]],"date-time":"2026-06-06T08:15:40Z","timestamp":1780733740133,"version":"3.54.1"},"reference-count":18,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2005,6,15]],"date-time":"2005-06-15T00:00:00Z","timestamp":1118793600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Birth Defects Research"],"published-print":{"date-parts":[[2005,7]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>BACKGROUND<\/jats:title><jats:p>The risk of having a child with a neural tube defect (NTD) can be reduced by maternal, periconceptional supplementation with folic acid, but the underlying folate\u2010dependent protective mechanism remains unclear. <jats:italic>N<\/jats:italic>\u2010acetyltransferase 1 is involved in acetylation of aromatic and heterocyclic amines and the catabolism of folates. Hence, functional polymorphisms in <jats:italic>NAT1<\/jats:italic>, the gene encoding <jats:italic>N<\/jats:italic>\u2010acetyltransferase 1, are plausible risk factors for NTDs. Such variants could exert an influence on the risk of NTDs via their role in acetylation or folate catabolism and could act through the maternal or the embryonic genotype.<\/jats:p><\/jats:sec><jats:sec><jats:title>METHODS<\/jats:title><jats:p><jats:italic>NAT1<\/jats:italic> C1095A genotypes and information on maternal, periconceptional multivitamin use and smoking were obtained as part of a family\u2010based study of spina bifida. Associations between spina bifida and the embryonic and maternal <jats:italic>NAT1<\/jats:italic> C1095A genotypes, and potential <jats:italic>NAT1<\/jats:italic> C1095A genotype\u2013exposure interactions were evaluated using log\u2010linear modeling.<\/jats:p><\/jats:sec><jats:sec><jats:title>RESULTS<\/jats:title><jats:p>The analyses provided no evidence that the embryonic or maternal <jats:italic>NAT1<\/jats:italic> C1095 genotypes influence the risk of spina bifida independently, or through interactions with maternal use of multivitamins. There was evidence that the embryonic, and possibly the maternal, <jats:italic>NAT1<\/jats:italic> C1095A genotype influence the risk of spina bifida via interactions with maternal smoking status.<\/jats:p><\/jats:sec><jats:sec><jats:title>CONCLUSIONS<\/jats:title><jats:p>The genotype for the <jats:italic>NAT1<\/jats:italic> C1095A polymorphism does not appear to be an independent risk factor for spina bifida. However, the results of these analyses provide preliminary evidence that this polymorphism may be associated with the risk of spina bifida in the offspring of women who smoke during early pregnancy. Birth Defects Research (Part A), 2005. \u00a9 2005 Wiley\u2010Liss, Inc.<\/jats:p><\/jats:sec>","DOI":"10.1002\/bdra.20143","type":"journal-article","created":{"date-parts":[[2005,6,15]],"date-time":"2005-06-15T17:46:41Z","timestamp":1118857601000},"page":"512-516","source":"Crossref","is-referenced-by-count":39,"title":["The <i>NAT1<\/i> C1095A polymorphism, maternal multivitamin use and smoking, and the risk of spina bifida"],"prefix":"10.1002","volume":"73","author":[{"given":"Liselotte E.","family":"Jensen","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Katy","family":"Hoess","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alexander S.","family":"Whitehead","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Laura E.","family":"Mitchell","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2005,6,15]]},"reference":[{"key":"e_1_2_6_2_1","first-page":"5226","article-title":"Polymorphism in the N\u2010acetyltransferase 1 (NAT1) polyadenylation signal: association of NAT1*10 allele with higher N\u2010acetylation activity in bladder and colon tissue","volume":"55","author":"Bell DA","year":"1995","journal-title":"Cancer Res"},{"key":"e_1_2_6_3_1","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199212243272602"},{"key":"e_1_2_6_4_1","first-page":"29","article-title":"Molecular genetics and epidemiology of the NAT1 and NAT2 acetylation polymorphisms","volume":"9","author":"Hein DW","year":"2000","journal-title":"Cancer Epidemiol Biomarkers Prev"},{"key":"e_1_2_6_5_1","first-page":"1425","article-title":"Pharmacogenetics of the arylamine N\u2010acetyltransferases: a symposium in honor of Wendell W. 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