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1 9th August 08:16
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Posts: 1
Default Milk whey protein / iron

Can J Cardiol. 2003 Sep;19(10):1163-1168. Links

Milk whey protein decreases oxygen free radical production in a murine model of
chronic iron-overload cardiomyopathy.

Bartfay WJ, Davis MT, Medves JM, Lugowski S.

Faculty of Nursing, University of Windsor, Windsor, Canada.

BACKGROUND: Chronic iron overload is a major cause of organ failure worldwide,
but its pathogenesis remains to be elucidated. OBJECTIVES: 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 hex****, 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 hex****
(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, hex**** 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). CONCLUSION: 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.

PMID: 14532942 [PubMed - as supplied by publisher]


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