title: Human milk enhances antioxidant defenses against hydroxyl radical aggression in preterm infants.
abstract: BACKGROUND
  Preterm infants endowed with an immature antioxidant defense system are prone to oxidative stress. Hydroxyl radicals are very aggressive reactive oxygen species that lack specific antioxidants. These radicals cannot be measured directly, but oxidation byproducts of DNA or phenylalanine in urine are reliable markers of their activity. Human milk has a higher antioxidant capacity than formula.
  
  
  OBJECTIVE
  We hypothesized that oxidative stress associated with prematurity could be diminished by feeding human milk.
  
  
  METHODS
  We recruited a cohort of stable preterm infants who lacked perinatal conditions associated with oxidative stress; were not receiving prooxidant or antioxidant drugs, vitamins, or minerals before recruitment; and were fed exclusively human milk (HM group) or preterm formula (PTF group). Collected urine was analyzed for oxidative bases of DNA [8-hydroxy-2'-deoxyguanosine (8-oxodG)/2'-deoxyguanosine (2dG) ratio] and oxidative derivatives of phenylalanine [ortho-tyrosine (o-Tyr)/Phe ratio] by HPLC coupled to tandem mass spectrometry. Healthy term newborn infants served as control subjects.
  
  
  RESULTS
  Both preterm groups eliminated greater amounts of metabolites than did the control group. However, the PTF group eliminated significantly (P < 0.02) higher amounts of 8-oxodG (8-oxodG/2dG ratio: 10.46 +/- 3.26) than did the HM group (8-oxodG/2dG ratio: 9.05 +/- 2.19) and significantly (P < 0.01) higher amounts of o-Tyr (o-Tyr/Phe ratio: 14.90 +/- 3.75) than did the HM group (o-Tyr/Phe ratio: 12.53 +/- 3.49). When data were lumped together independently of the type of feeding received, a significant correlation was established between the 8-oxodG/2dG and o-Tyr/Phe ratios in urine, dependent on gestational age and birth weight.
  
  
  CONCLUSIONS
  Prematurity is associated with protracted oxidative stress, and human milk is partially protective.
authors.affiliation: Division of Neonatology, Hospital Universitario Materno Infantil La Fe, Valencia, Spain.
authors.forename: Ana
authors.initials: A
authors.lastname: Ledo
authors.forename: Alessandro
authors.initials: A
authors.lastname: Arduini
authors.forename: Miguel A
authors.initials: MA
authors.lastname: Asensi
authors.forename: Juan
authors.initials: J
authors.lastname: Sastre
authors.forename: Raquel
authors.initials: R
authors.lastname: Escrig
authors.forename: María
authors.initials: M
authors.lastname: Brugada
authors.forename: Marta
authors.initials: M
authors.lastname: Aguar
authors.forename: Pilar
authors.initials: P
authors.lastname: Saenz
authors.forename: Maximo
authors.initials: M
authors.lastname: Vento
mesh_terms: D000080242:8-Hydroxy-2'-Deoxyguanosine; D000704:Analysis of Variance; D000975:Antioxidants / Q000378:metabolism / Q000494:pharmacology*; D015415:Biomarkers / Q000652:urine; D016022:Case-Control Studies; D002851:Chromatography, High Pressure Liquid; D015331:Cohort Studies; D004249:DNA Damage; D003849:Deoxyguanosine / Q000031:analogs & derivatives / Q000652:urine; D005260:Female; D005865:Gestational Age; D006801:Humans; D017665:Hydroxyl Radical; D041943:Infant Formula / Q000737:chemistry; D007227:Infant Nutritional Physiological Phenomena / Q000502:physiology*; D007231:Infant, Newborn; D007234:Infant, Premature; D008297:Male; D008895:Milk, Human / Q000737:chemistry*; D018384:Oxidative Stress / Q000187:drug effects*; D010649:Phenylalanine / Q000031:analogs & derivatives / Q000652:urine; D017382:Reactive Oxygen Species / Q000378:metabolism; D053719:Tandem Mass Spectrometry
chemical_list: D000975:Antioxidants; D015415:Biomarkers; D017382:Reactive Oxygen Species; D017665:Hydroxyl Radical; D010649:Phenylalanine; D000080242:8-Hydroxy-2'-Deoxyguanosine; D003849:Deoxyguanosine