Raghuveer Talkad S, McGuire Erin M, Martin Sean M, Wagner Brett A, Rebouché Charles J, Buettner Garry R, Widness John A
Department of Pediatrics, The University of Iowa, Iowa City, Iowa 52242, USA.
Pediatr Res. 2002 Dec;52(6):964-72. doi: 10.1203/00006450-200212000-00024.
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.
自由基损伤被认为在低出生体重早产儿的多种疾病发病机制中起重要作用，这些疾病包括早产儿视网膜病变和坏死性小肠结肠炎。由于铁是自由基介导的氧化反应中一种已知的催化剂，因此本体外研究的目的是确定在暴露于空气后：1）婴儿配方奶粉中存在的铁，或作为药用铁添加到母乳或配方奶粉中的铁，或人乳强化剂中含有的铁，是否会增加自由基和脂质过氧化产物；2）添加到配方奶粉或母乳中的重组人乳铁蛋白是否会减弱铁介导的自由基形成和脂质过氧化。在向配方奶粉和母乳中添加药用铁之前，在配方奶粉中观察到显著更多的抗坏血酸和α - 羟乙基自由基产生以及更多的脂质过氧化产物（即硫代巴比妥酸反应性物质、丙二醛和乙烷）。在向配方奶粉或母乳中添加药用铁后，自由基和脂质过氧化产物进一步增加。当向母乳中添加含铁的人乳强化剂时，自由基也会增加。相比之下，当存在药用铁或人乳强化剂时，向配方奶粉或母乳中添加脱辅基重组人乳铁蛋白会降低氧化产物的水平。我们推测，与母乳相比，配方奶粉中铁浓度更高且缺乏乳铁蛋白会导致体外产生更多的自由基和脂质过氧化产物。含乳铁蛋白的配方奶粉经肠道给予早产儿是否会在体内产生较少的自由基还有待确定。
