title: Birth weight of Korean infants is affected by the interaction of maternal iron intake and GSTM1 polymorphism.
abstract: Excessive iron consumption during pregnancy can lead to increased oxidative stress in the maternal body, which may result in adverse pregnancy outcomes. Glutathione S-transferases (GSTs) originate from a superfamily of detoxifying enzymes that play a role in reducing xenobiotic compounds and oxidative stress. The aim of this study was to determine the relationship among GST gene expression, maternal iron intake during pregnancy, and neonatal birth weight. The study participants were 1087 Korean gravidas and their newborns recruited for the Mothers and Children's Environmental Health study between 2006 and 2010. A 24-h dietary recall interview was conducted to estimate iron intake; additional intake through nutritional supplements was thoroughly investigated. Deletion polymorphisms of GSTM1 and GSTT1 were genotyped using PCR. Dietary iron consumption during pregnancy was positively associated with birth weight in pregnant women who were GSTM1-present after adjustment for the following covariates: maternal age, prepregnancy BMI, mother's education level, log-transformed urinary cotinine level, infant gender, gestational age at term, log-transformed energy intake, parity, and the use of folic acid supplements (P < 0.05). There were interactions between the GSTM1 genotype and iron intakes from animal foods (P < 0.05), diet (P < 0.05), and diet with supplements (P < 0.05). No relationship was found between maternal iron intake and birth weight for the GSTT1 polymorphism. This study demonstrates that increased iron consumption during pregnancy may improve infant birth weight for mothers who are GSTM1-present, but it might not be beneficial for mothers with the GSTM1-null genotype.
authors.affiliation: Department of Nutritional Science and Food Management, College of Medicine, Ewha Womans University, Seoul, Korea.
authors.forename: Jinhee
authors.initials: J
authors.lastname: Hur
authors.forename: Hyesook
authors.initials: H
authors.lastname: Kim
authors.forename: Eun-Hee
authors.initials: EH
authors.lastname: Ha
authors.forename: Hyesook
authors.initials: H
authors.lastname: Park
authors.forename: Mina
authors.initials: M
authors.lastname: Ha
authors.forename: Yangho
authors.initials: Y
authors.lastname: Kim
authors.forename: Yun-Chul
authors.initials: YC
authors.lastname: Hong
authors.forename: Namsoo
authors.initials: N
authors.lastname: Chang
mesh_terms: D000328:Adult; D018798:Anemia, Iron-Deficiency / Q000503:physiopathology / Q000517:prevention & control; D001724:Birth Weight; D015331:Cohort Studies; D019587:Dietary Supplements / Q000009:adverse effects; D005260:Female; D005317:Fetal Growth Retardation / Q000209:etiology / Q000235:genetics / Q000378:metabolism / Q000517:prevention & control; D017353:Gene Deletion; D056726:Genetic Association Studies; D005982:Glutathione Transferase / Q000172:deficiency / Q000235:genetics* / Q000378:metabolism; D006801:Humans; D019266:Iron, Dietary / Q000008:administration & dosage* / Q000009:adverse effects / Q000627:therapeutic use; D039382:Maternal Nutritional Physiological Phenomena; D018384:Oxidative Stress; D011110:Polymorphism, Genetic; D011247:Pregnancy; D011248:Pregnancy Complications / Q000503:physiopathology / Q000517:prevention & control; D011446:Prospective Studies; D056910:Republic of Korea
chemical_list: D005982:Glutathione Transferase; D019266:Iron, Dietary; C413545:glutathione S-transferase T1