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(Received for publication, November 26, 1996, and in revised form, February 28, 1997)
From the Vitamin C (ascorbic acid, AA) can act as an
antioxidant or a pro-oxidant in vitro, depending on the
absence or the presence, respectively, of redox-active metal ions. Some
adults with iron-overload and some premature infants have potentially
redox-active, bleomycin-detectable iron (BDI) in their plasma. Thus, it
has been hypothesized that the combination of AA and BDI causes
oxidative damage in vivo. We found that plasma of preterm
infants contains high levels of AA and F2-isoprostanes,
stable lipid peroxidation end products. However,
F2-isoprostane levels were not different between those infants with BDI (138 ± 51 pg/ml, n = 19) and
those without (126 ± 41 pg/ml, n = 10), and the
same was true for protein carbonyls, a marker of protein oxidation
(0.77 ± 0.31 and 0.68 ± 0.13 nmol/mg protein,
respectively). Incubation of BDI-containing plasma from preterm infants
did not result in detectable lipid hydroperoxide formation (
Volume 272, Number 25,
Issue of June 20, 1997
pp. 15656-15660
©1997 by The American Society for Biochemistry and Molecular Biology, Inc.
,
,
and
Joint Program in Neonatology, Harvard
Medical School, Boston, Massachusetts 02115, the ¶ International
Antioxidant Research Center, King's College, London SW3 6LX, United
Kingdom, the 
Vanderbilt University School of Medicine,
Nashville, Tennessee 37232, and the § Evans Memorial
Department of Medicine, Whitaker Cardiovascular Institute, Boston
University School of Medicine, Boston, Massachusetts 02118
10
nM cholesteryl ester hydroperoxides) as long as AA
concentrations remained high. Furthermore, when excess iron was added
to adult plasma, BDI became detectable, and endogenous AA was rapidly
oxidized. Despite this apparent interaction between excess iron and
endogenous AA, there was no detectable lipid peroxidation as long as AA
was present at >10% of its initial concentration. Finally, when iron
was added to plasma devoid of AA, lipid hydroperoxides were formed
immediately, whereas endogenous and exogenous AA delayed the onset of
iron-induced lipid peroxidation in a dose-dependent manner.
These findings demonstrate that in iron-overloaded plasma, AA acts an
antioxidant toward lipids. Furthermore, our data do not support the
hypothesis that the combination of high plasma concentrations of AA and
BDI, or BDI alone, causes oxidative damage to lipids and proteins
in vivo.
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