title: Pregnancy outcome in ethanol-treated mice with folic acid supplementation in saccharose.
abstract: BACKGROUND
  Maternal folic acid deficiency is the most important metabolic factor in the etiology of neural tube defects (NTD) and is reduced by ethanol, which is extensively consumed by young women.
  
  
  OBJECTIVE
  The objective of the study was to determine whether folic acid supplementation in dietary saccharose is efficient in the prevention NTD induced by ethanol in fetuses of Swiss mice.
  
  
  METHODS
  Pregnant mice were divided into four groups of six animals each: control (C), ethanol (E), deficient-supplemented (DS), and deficient-supplemented + ethanol (DSE). Groups C and E received commercial mouse chow (containing 3 mg/kg folic acid) throughout the experiment, while groups DS and DSE received a folic acid-free diet with the addition of saccharose supplemented with folic acid (2 mg/kg folic acid) in water. Group E and DSE animals received ethanol (4 g/kg) administered intraperitoneally from the seventh to the ninth gestational day (gd) and were euthanized on the 18th gd, while groups C and DS received saline.
  
  
  RESULTS
  Congenital anomalies were observed in groups E and DSE. The fetal weight and length of the animals in group E were lower than in groups C and DS and, in group DSE, were lower than in groups C and DS. The placental diameter of group E was smaller than that of group C, and the placental weight of group C animals was lower than that of groups E, DSE, and DS.
  
  
  CONCLUSIONS
  The study demonstrated that dietary supplementation with folate in saccharose is an accessible means of consumption that could be further diffused but in an increased dose than recommended to reduce the teratogenic effects of ethanol.
authors.affiliation: Department of Pathology, Faculty of Medicine of Ribeirão Preto, University of São Paulo, Ribeirão Preto, SP, Brazil.
authors.forename: M Y
authors.initials: MY
authors.lastname: Yanaguita
authors.forename: C M
authors.initials: CM
authors.lastname: Gutierrez
authors.forename: C N M
authors.initials: CN
authors.lastname: Ribeiro
authors.forename: G A
authors.initials: GA
authors.lastname: Lima
authors.forename: H R
authors.initials: HR
authors.lastname: Machado
authors.forename: L C
authors.initials: LC
authors.lastname: Peres
mesh_terms: D000014:Abnormalities, Drug-Induced / Q000517:prevention & control*; D000284:Administration, Oral; D000818:Animals; D002492:Central Nervous System Depressants / Q000008:administration & dosage / Q000633:toxicity; D019587:Dietary Supplements; D000431:Ethanol / Q000008:administration & dosage / Q000633:toxicity*; D005260:Female; D005317:Fetal Growth Retardation / Q000139:chemically induced / Q000517:prevention & control; D020567:Fetal Weight / Q000187:drug effects; D005492:Folic Acid / Q000008:administration & dosage / Q000737:chemistry / Q000627:therapeutic use*; D005865:Gestational Age; D007274:Injections, Intraperitoneal; D008297:Male; D018811:Maternal Exposure; D051379:Mice; D009436:Neural Tube Defects / Q000139:chemically induced / Q000517:prevention & control; D011247:Pregnancy; D011256:Pregnancy Outcome; D011297:Prenatal Exposure Delayed Effects / Q000139:chemically induced / Q000517:prevention & control; D013395:Sucrose / Q000737:chemistry*
chemical_list: D002492:Central Nervous System Depressants; D000431:Ethanol; D013395:Sucrose; D005492:Folic Acid