title: Goat milk supplemented with folic acid protects cell biomolecules from oxidative stress-mediated damage after anaemia recovery in comparison with cow milk.
abstract: BACKGROUND
  Fe overload is a common consequence of the anaemia treatment, increasing the oxidative stress and promoting the accumulation of damaged biomolecules, with the subsequently impairment of cell functions. Oxidative stress and the role of folic acid preventing free radical damage have been extensively studied; nevertheless, no studies are available about the influence of folic acid-supplemented goat milk consumption on the oxidative stress-mediated damage.
  
  
  OBJECTIVE
  The objective of the present study was to assess the influence of folic acid supplementation of goat milk- or cow milk-based diets, after Fe-overload treatment to palliate anaemia, on oxidative stress-mediated biomolecular damage in the liver, brain, erythrocytes, duodenal mucosa and plasma.
  
  
  METHODS
  Control and anaemic rats were fed goat milk- or cow milk-based diets, either with normal Fe or Fe overload (450 mg/kg), and normal folic acid (2 mg/kg) or folic acid supplemented (40 mg/kg) for 30 days.
  
  
  RESULTS
  During chronic Fe repletion, background DNA damage was significantly lower in anaemic rats fed folic acid-supplemented goat milk-based diet, as revealed by tail DNA (%), and folic acid-supplemented goat milk also had a beneficial effect, reducing the extent of lipid peroxidation in liver, plasma, erythrocytes and especially in brain and duodenal mucosa. Furthermore, protein oxidative damage was lower in anaemic rat duodenal mucosa for all goat milk-based diets.
  
  
  CONCLUSIONS
  Folic acid supplement in goat milk avoids the undesirable effects of Fe overload during anaemia recovery in all the tissues studied, especially in the liver and duodenal mucosa, which are the tissues with higher exposition to dietary Fe.
authors.affiliation: Department of Physiology, Faculty of Pharmacy and Institute of Nutrition and Food Technology "José Mataix", University of Granada, Campus Universitario de Cartuja, 18071, Granada, Spain.
authors.forename: Javier
authors.initials: J
authors.lastname: Díaz-Castro
authors.forename: Ana
authors.initials: A
authors.lastname: Sánchez-Alcover
authors.forename: Silvia
authors.initials: S
authors.lastname: Hijano
authors.forename: María J M
authors.initials: MJ
authors.lastname: Alférez
authors.forename: Teresa
authors.initials: T
authors.lastname: Nestares
authors.forename: Miguel
authors.initials: M
authors.lastname: Moreno
authors.forename: Margarita S
authors.initials: MS
authors.lastname: Campos
authors.forename: Inmaculada
authors.initials: I
authors.lastname: López-Aliaga
mesh_terms: D000740:Anemia / Q000188:drug therapy*; D000818:Animals; D001921:Brain / Q000187:drug effects / Q000378:metabolism; D002417:Cattle; D020552:Comet Assay; D019587:Dietary Supplements; D004912:Erythrocytes / Q000187:drug effects / Q000378:metabolism; D005293:Ferritins / Q000097:blood; D005492:Folic Acid / Q000494:pharmacology*; D006041:Goats; D006454:Hemoglobins / Q000187:drug effects / Q000378:metabolism; D019266:Iron, Dietary / Q000097:blood; D015227:Lipid Peroxidation / Q000187:drug effects; D008099:Liver / Q000187:drug effects / Q000378:metabolism; D008297:Male; D008892:Milk / Q000737:chemistry*; D018384:Oxidative Stress / Q000187:drug effects*; D020011:Protective Agents / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D014168:Transferrin / Q000378:metabolism
chemical_list: D006454:Hemoglobins; D019266:Iron, Dietary; D020011:Protective Agents; D017392:Thiobarbituric Acid Reactive Substances; D014168:Transferrin; D005293:Ferritins; D005492:Folic Acid