Lactoferrin in the Preterm Infants' Diet Attenuates Iron-Induced Oxidation Products

Raghuveer, Talkad S; McGuire, Erin M; Martin, Sebastian; Wagner, Brett A.; Rebouche, Charles J.; Buettner, Garry R.; Widness, John A.

doi:10.1203/00006450-200212000-00024

Cited by 70 publications

(35 citation statements)

References 46 publications

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“…Several of its components have been shown to be positively correlated to cerebral development2 including lactoferrin (Lf). Lf is an iron-binding glycoprotein3 with multiple biological functions (iron absorption, anti-inflammatory, immunomodulator, antioxidant, host defense mechanism, anticarcinogenicity) 4–9. It is produced by exocrine glands and released in mucosal secretions including at a high level in colostrum and maternal milk 10.…”

Section: Introductionmentioning

confidence: 99%

Lactoferrin during lactation protects the immature hypoxic‐ischemic rat brain

Looij

Ginet

Chatagner

et al. 2014

Ann Clin Transl Neurol

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ObjectiveLactoferrin (Lf) is an iron-binding glycoprotein secreted in maternal milk presenting anti-inflammatory and antioxidant properties. It shows efficient absorption into the brain from nutritional source. Brain injury frequently resulting from cerebral hypoxia-ischemia (HI) has a high incidence in premature infants with ensuing neurodevelopmental disabilities. We investigated the neuroprotective effect of maternal nutritional supplementation with Lf during lactation in a rat model of preterm HI brain injury using magnetic resonance imaging (MRI), brain gene, and protein expression.MethodsModerate brain HI was induced using unilateral common carotid artery occlusion combined with hypoxia (6%, 30 min) in the postnatal day 3 (P3) rat brain (24–28 weeks human equivalent). High-field multimodal MRI techniques were used to investigate the effect of maternal Lf supplementation through lactation. Expression of cytokine coding genes (TNF-α and IL-6), the prosurvival/antiapoptotic AKT protein and caspase-3 activation were also analyzed in the acute phase after HI.ResultsMRI analysis demonstrated reduced cortical injury in Lf rats few hours post-HI and in long-term outcome (P25). Lf reduced HI-induced modifications of the cortical metabolism and altered white matter microstructure was recovered in Lf-supplemented rats at P25. Lf supplementation significantly decreased brain TNF-α and IL-6 gene transcription, increased phosphorylated AKT levels and reduced activation of caspase-3 at 24 h post-injury.InterpretationLf given through lactation to rat pups with cerebral HI injury shows neuroprotective effects on brain metabolism, and cerebral gray and white matter recovery. This nutritional intervention may be of high interest for the clinical field of preterm brain neuroprotection.

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Section: Introductionmentioning

confidence: 99%

Lactoferrin during lactation protects the immature hypoxic‐ischemic rat brain

Looij

Ginet

Chatagner

et al. 2014

Ann Clin Transl Neurol

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“…Determination of Thiobarbituric Acid-Reactive Substances (TBA) TBA value was measured according to Raghuveer et al (2002) and Friel et al (2007) with modification. In brief, 1 g of milk powder sample was mixed with 9 mL of deionised water and 10 mL of 20% (w/v) trichloroacetic acid (TCA) in a glass screw-top test tube, vortexed, and centrifuged at 8,000 rpm for 15 min to precipitate its proteins.…”

Section: Introductionmentioning

confidence: 99%

Comprehensive Stability Evaluation of Iron-Fortified Milk Powder

Lee

Khoo

et al. 2012

FSTR

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Well-documented stability studies on iron-fortified food are limited due to the complexity of ingredients and processing methods. Here, we performed a comprehensive stability evaluation on iron-fortified milk powder with various iron contents and packaging methods. Free fatty acid increased gradually over a 9 month storage period in both iron-fortified and non iron-fortified formulas, regardless of the packaging methods. Thiobarbituric acid (TBA) value level remained stable in anaerobic packaging condition but increased in aerobic condition. Lipid oxidation was highest in Fe(III)-fortified formula. We showed significant increment of browning reactions, moisture and water activities in aerobic condition, especially in iron-fortified formulas, while no significant changes in anaerobic-packaged formulas. Scanning electron microscopy (SEM) showed highest porosity in Fe(III)-fortified formula. Our results showed Fe(III)-fortified formula has the lowest stability in aerobic condition but its stability improved significantly with vacuum/anaerobic packaging. Thus, our studies contribute to understanding and improving the processing and quality of iron-fortified food.

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“…We have shown that ferrous fumarate produces minimal or no oxidative stress in vitro compared with ferrous sulfate. 10 Lactoferrin in HM attenuates iron-induced oxidation products in vitro. 10 Because all of the infants in the study of Braekke et al were fed HM, the level of iron-induced oxidative stress would be expected to be attenuated by lactoferrrin.…”

Section: To the Editormentioning

confidence: 99%

Iron supplements and oxidative stress in very low birth weight infants

Raghuveer

Buettner

2008

The Journal of Pediatrics

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We congratulate Braekke et al on their recent report. 1 The practice in Norway of administering iron supplementation to very low birth weight (VLBW) infants with 18 mg/day of ferrous fumarate from age 6 weeks is based on a 1955 study of 26 infants by Gairdner et al, 2 in which 50% received 60 mg of ferrous sulfate 3 times a day from age 2 or 3 weeks and 50% received the same dose of iron when their hemoglobin level fell to 11 g/100 mL. Gairdner et al concluded that iron supplements given to VLBW infants starting at age 3 weeks could mitigate anemia.Today, VLBW infants who survive are more premature, have poorer antioxidant defense systems, 3,4 and receive more red cell transfusions. Braekke et al have correctly raised the question of whether it is wise practice to continue high iron supplementation in VLBW infants. We would like to comment on whether their findings should affect the clinical care of VLBW infants in the United States.Braekke et al studied healthy and stable VLBW infants with a median weight of 1785 g at age 5 weeks. They excluded infants requiring >30% oxygen and/or mechanical ventilation. However, it is the "sick" and unstable VLBW infants who are at higher risk for developing severe bronchopulmonary dysplasia, necrotizing enterocolitis, and retinopathy of prematurity. Oxidative stress contributes to each of these morbidities. 5 Administration of ferrous iron, which can initiate the oxidation cascade, 6 may result in overloaded antioxidation capacity. Studies of these sick and unstable infants are needed to provide information on oxidative stress due to iron supplementation.The authors draw their conclusions based on 1 week of iron supplementation. The question remains open as to whether oxidative stress from high doses of iron supplements would increase with longer exposure periods that reflect real life situations.In this study, the median plasma ferritin level dropped from 84 to 59 µg/L between weeks 5 and 6 and increased to 63 µg/L by the end of week 7. None of the infants had iron-deficiency anemia, defined as plasma ferritin level <10 µg/L. 7 Most of the infants with birth weight <1000 g had received red cell transfusions, which resulted in higher serum ferritin levels before the initiation of iron supplementation. Thus, the risk of iron-deficiency anemia in HHS Public Access

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Lactoferrin in the Preterm Infants' Diet Attenuates Iron-Induced Oxidation Products

Cited by 70 publications

References 46 publications

Lactoferrin during lactation protects the immature hypoxic‐ischemic rat brain

Lactoferrin during lactation protects the immature hypoxic‐ischemic rat brain

Comprehensive Stability Evaluation of Iron-Fortified Milk Powder

Iron supplements and oxidative stress in very low birth weight infants

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