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Lactoferrin in the preterm infants' diet attenuates iron-induced oxidation products
Talkad S Raghuveer1, Erin M McGuire, Sean M Martin
1Department of Pediatrics, The University of Iowa, Iowa City, Iowa 52242, USA. traghuveer@kumc.edu
Insights
Iron in infant formula increases harmful free radicals and lipid peroxidation. Adding lactoferrin to formula or human milk reduces these oxidative products, suggesting a protective role for lactoferrin in premature infant nutrition.
Area of Science:
- Biochemistry
- Neonatal Nutrition
- Oxidative Stress
Background:
- Free radical injury is implicated in diseases of premature infants, such as retinopathy of prematurity and necrotizing enterocolitis.
- Iron catalyzes free radical-mediated oxidation reactions, raising concerns about its role in infant nutrition.
Purpose of the Study:
- To investigate if iron in infant formula or added iron sources increases free radical and lipid peroxidation products in vitro.
- To determine if recombinant human lactoferrin can reduce iron-mediated free radical formation and lipid peroxidation in infant formulas and human milk.
Main Methods:
- In vitro studies exposing infant formula and human milk to air, with and without added medicinal iron or iron-containing human milk fortifier.
- Measurement of free radical production (ascorbate and alpha-hydroxyethyl radicals) and lipid peroxidation products (thiobarbituric acid reactive substances, malondialdehyde, ethane).
- Assessment of the effect of adding apo-recombinant human lactoferrin on oxidative product levels.
Main Results:
- Infant formula exhibited higher baseline levels of free radical and lipid peroxidation products compared to human milk.
- Addition of medicinal iron or iron-containing human milk fortifier significantly increased oxidative products in both formula and human milk.
- Apo-recombinant human lactoferrin addition effectively decreased oxidative product levels in the presence of iron.
Conclusions:
- Higher iron concentration and absence of lactoferrin in infant formula contribute to greater in vitro free radical generation and lipid peroxidation.
- Recombinant human lactoferrin demonstrates potential to mitigate iron-induced oxidative stress in infant nutrition.
- Further in vivo studies are needed to confirm the protective effects of lactoferrin in preterm infants receiving iron-fortified formula.
Abstract:
Free radical injury is thought to play a significant role in the pathogenesis of several disease processes in low birth weight premature infants including retinopathy of prematurity and necrotizing enterocolitis. Because iron is a known catalyst in free radical-mediated oxidation reactions, the objectives of the present in vitro studies were to determine whether after exposure to air 1) iron present in infant formula, or that added to human milk or formula as medicinal iron or as iron contained in human milk fortifier, increases free radical and lipid peroxidation products; and 2) recombinant human lactoferrin added to formula or human milk attenuates iron-mediated free radical formation and lipid peroxidation. Before adding medicinal iron to formula and human milk, significantly more ascorbate and alpha-hydroxyethyl radical production and more lipid peroxidation products (i.e. thiobarbituric acid reactive substances, malondialdehyde, and ethane) were observed in formula. After the addition of medicinal iron to either formula or human milk, further increases were observed in free radical and lipid peroxidation products. When iron-containing human milk fortifier was added to human milk, free radicals also increased. In contrast, the addition of apo-recombinant human lactoferrin to formula or human milk decreased the levels of oxidative products when medicinal iron or human milk fortifier was present. We speculate that the presence of greater concentration of iron and the absence of lactoferrin in formula compared with human milk results in greater in vitro generation of free radicals and lipid peroxidation products. Whether iron-containing formula with lactoferrin administered enterally to preterm infants will result in less free radical generation in vivo has yet to be established.