title: Milk whey protein decreases oxygen free radical production in a murine model of chronic iron-overload cardiomyopathy.
abstract: BACKGROUND
  Chronic iron overload is a major cause of organ failure worldwide, but its pathogenesis remains to be elucidated.
  
  
  OBJECTIVE
  To examine in an experimental murine model of iron-overload cardiomyopathy the relation between milk whey protein and, first, the production of reactive oxygen free radical species and, second, antioxidant reserve status.
  
  
  METHODS
  B6D2F1 mice were randomly assigned to four treatment groups (n=8 per treatment group): placebo control; iron only; whey only; and iron with whey. Reactive oxygen free radical species in the heart were quantified by the cytotoxic aldehydes malondialdehyde (MDA), 4-hydroxy-nonenal (HNE) and hexanal, while antioxidant reserve status was quantified by glutathione (GSH) and glutathione peroxidase (GPx) activity in the heart tissue.
  
  
  RESULTS
  Significantly decreased concentrations (pmol/100 mg wet weight tissue) of MDA (2468+/-261), HNE (912+/-38) and hexanal (5385+/-927) were observed in the heart tissue of the group receiving iron with whey, in comparison with the iron-only treatment group (MDA 9307+/-387, HNE 1416+/-157, hexanal 14,874+/-2955; P<0.001). Significantly increased GPx (141+/-38 IU/L) and GSH (521+/-136 IU/L) activity were observed in mice receiving iron with whey, in comparison with mice receiving iron only (GPx 100+/-10 IU/L, GSH 446+/-33 IU/L; P<0.001).
  
  
  CONCLUSIONS
  Mice receiving iron treatments with whey supplementation had significantly lower concentrations of cytotoxic aldehydes and significantly higher cardiac levels of GPx and GSH activity than did iron-only treated mice. Additional basic research is warranted to examine the exact mechanisms by which milk whey protein protects the heart.
authors.affiliation: Faculty of Nursing, University of Windsor, Windsor, Ontario, Canada. wbartfay@uwindsor.ca
authors.forename: Wally J
authors.initials: WJ
authors.lastname: Bartfay
authors.forename: Matthew T
authors.initials: MT
authors.lastname: Davis
authors.forename: Jennifer M
authors.initials: JM
authors.lastname: Medves
authors.forename: Stan
authors.initials: S
authors.lastname: Lugowski
mesh_terms: D000447:Aldehydes / Q000378:metabolism; D000818:Animals; D009202:Cardiomyopathies / Q000378:metabolism*; D002908:Chronic Disease; D004195:Disease Models, Animal; D005609:Free Radicals / Q000378:metabolism*; D005979:Glutathione Peroxidase / Q000378:metabolism; D019190:Iron Overload / Q000378:metabolism*; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains; D008894:Milk Proteins / Q000494:pharmacology*; D009206:Myocardium / Q000201:enzymology; D011897:Random Allocation
chemical_list: D000447:Aldehydes; D005609:Free Radicals; D008894:Milk Proteins; C010463:n-hexanal; D005979:Glutathione Peroxidase