Intraerythrocyte nonprotein-bound iron and plasma malondialdehyde in the hypoxic newborn

Buonocore, Giuseppe; Zani, S; Perrone, Serafina; Caciotti, Barbara; Bracci, Rodolfo

doi:10.1016/s0891-5849(98)00126-9

Cited by 87 publications

(53 citation statements)

References 27 publications

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“…Additional pathways can contribute to expose preterm newborns to FR damage in the postnatal period. In the first week of life, preterm babies are at high risk for oxidative stress because of postnatal environmental oxygen concentrations, which are higher than those of the intrauterine environment, therapeutic use of oxygen, and elevated non-protein-bound iron concentrations in red blood cells and plasma (10,26,27). Activation of polymorphonuclear leukocytes, often associated with preterm labor and delivery, can be harmful because activated neutrophils produce a flood of FR (28).…”

Section: Discussionmentioning

confidence: 99%

“…Thirty-four of the 49 newborns were regarded as hypoxic if they fulfilled at least two of the following criteria: pH Յ 7.20 in umbilical vein, Apgar score Յ 6 at 5 min, and fraction of inspired oxygen Ն 0.4 needed to achieve oxygen saturation Ն 86% at birth. These criteria, less severe than those established by the American College of Obstetricians and Gynecologists to define newborns with birth asphyxia (9), were chosen, as in previous papers of ours (8,10,11), to evaluate all hypoxic babies, even those with mild hypoxia. Ten of 34 hypoxic babies were reanalyzed separately to verify whether stricter criteria of hypoxia (pH Ͻ 7.15 in umbilical vein, Apgar score Ͻ 5 at 5 min) changed our results.…”

Section: Patientsmentioning

confidence: 99%

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Oxidative Stress in Preterm Neonates at Birth and on the Seventh Day of Life

Buonocore¹

2002

Pediatric Research

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Previous studies have demonstrated increased oxidative damage to proteins and increased lipid peroxidation products in the plasma of hypoxic newborns at birth. We tested the hypothesis that hypoxic preterm newborns are at increased risk for oxidative stress in the first week of life. Heparinized blood samples of 34 hypoxic and 15 control preterm newborns were obtained at birth from the umbilical vein immediately after delivery and from a peripheral vein on postnatal d 7. Plasma levels of hypoxanthine, total hydroperoxide (TH), and advanced oxidation protein products (AOPP) were measured in cord blood and blood drawn on d 7. Hypoxanthine, TH, and AOPP levels were significantly higher in cord and d 7 blood samples of hypoxic newborn than control infants. Statistically significant correlations were observed between AOPP and hypoxanthine and between AOPP and TH plasma levels on d 7. AOPP and TH plasma levels significantly increased from cord to d 7 blood in neonates without hypoxia. These findings show that the oxidative stress observed in cord blood of hypoxic preterm newborns is still higher than control infants on d 7. The significant increase in TH and AOPP levels in nonhypoxic preterm newborns at the end of the first postnatal week indicates that damage caused by free radicals also occurs in nonhypoxic babies with normal clinical course. In summary, TH and AOPP production is prolonged for several days after birth in hypoxic preterm babies. The risk of free radical damage is lower but still exists in preterm neonates with normal clinical course. Perinatal hypoxic-ischemic injury is an important cause of neonatal morbidity. Numerous experimental studies have demonstrated FR production and oxidative damage caused by hypoxia in fetal life (1-3). Although the clinical consequences of hypoxia are readily observed, the specific biochemical processes preceding the onset of FR damage are not well understood. Oxidative stress exists and tissue damage is possible when there are low levels of antioxidants or increased FR activity (4). Newborns and particularly preterm infants are at high risk for oxidative stress and are very susceptible to oxidative damage by FR (5). Indeed, there is evidence of an imbalance between antioxidant and oxidant-generating systems, which causes oxidative damage (6). Birth is an oxidative challenge for the newborn. The sharp postnatal transition from the relatively low oxygen intrauterine environment to the significantly higher oxygen extrauterine environment exposes the newborn to FR. The increase in FR generation is exacerbated by the low efficiency of natural antioxidant systems in the newborn, especially if preterm, predisposing it to oxidative damage (7). High FR generation and protein oxidation products have been detected in the plasma of preterm hypoxic newborns at birth (8). Sick preterm newborns may be particularly exposed to FR in the first postnatal week because of frequent intensive care, involving oxygen supply, assisted ventilation, surfactant administration, and total parenteral n...

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Section: Discussionmentioning

confidence: 99%

Section: Patientsmentioning

confidence: 99%

Oxidative Stress in Preterm Neonates at Birth and on the Seventh Day of Life

Buonocore¹

2002

Pediatric Research

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“…Whatever the origin, iron release and FR generation expose newborns with poorly developed antioxidant systems to oxidative damage. We previously demonstrated that preterm babies had higher concentrations of NPBI and lower antioxidant responses than term babies (13,30,31). A strong correlation exists between NPBI concentration and gestational age at birth.…”

Section: Plasma Protein Oxidation At Birthmentioning

confidence: 96%

“…It attacks all classes of biologic macromolecules depolymerizing polysaccharides, breaking DNA strands, inactivating enzymes, and peroxidating lipids (9 -11). NPBI is released from hemoglobin when erythrocytes are challenged by an oxidative stress (12,13). The newborn is very susceptible to NPBI-induced oxidative stress (14).…”

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Nonprotein-Bound Iron and Plasma Protein Oxidative Stress at Birth

et al. 2005

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We previously reported plasma nonprotein-bound iron (NPBI) as a reliable early indicator of intrauterine oxidative stress (OS) and brain injury. We tested the hypothesis that albumin, an NPBI serum carrier, is the major target of NPBIinduced OS. Twenty-four babies were randomly selected from 384 newborns constituting the final cohort of a prospective study undertaken to evaluate the predictive role of NPBI in cord blood for neurodevelopmental outcome. Twelve were selected in the group with lowest NPBI levels (0 -1.16 M) and good neurodevelopmental outcome and 12 in the group with highest NPBI levels (Ն15.2 M) and poor neurodevelopmental outcome. Protein carbonyl groups were identified in cord blood samples by two-dimensional polyacrylamide gel electrophoresis (2D-PAGE) and Western blotting with anti-2,4-dinitrophenyl (DNP) antibodies. Two series of immunoreactive spots, corresponding to serum albumin and ␣-fetoprotein, were found only in the group with highest NPBI levels. We found an association between NPBI and carbonylated proteins in babies with highest NPBI levels. Since NPBI may produce hydroxyl radicals through the Fenton reaction, the major target of OS induced by NPBI is its carrier: albumin. Oxidation of albumin can be expected to decrease plasma antioxidant defenses and increase the likelihood of tissue damage due to OS in the newborns. Proteins are an important target for oxidative modification; oxidatively modified forms of proteins accumulate during OS induced by free radical (FR) generation. The modification is a consequence of oxidation of amino acid residues on proteins to form protein CG.CG form during normal aging (1) and in neonates receiving oxygen ventilation (2). Protein CG content is the most widely used marker of oxidative modification of the proteins and the term carbonyl stress has been used to describe excess formation of CG under physiologic and pathologic conditions, such as hypoxia-induced NPBI (3-6).NPBI indicate a low molecular mass iron form, free of high-affinity binding to transferrin, that seems to occur in plasma, complexed to citrate, lactate, or phosphate or loosely bound to albumin or other proteins (7). In blood, NPBI causes release of hydroxyl radical (OH·) by superoxide and hydrogen peroxide, possibly via iron-oxygen complexes (8). OH· is an extremely powerful oxidizing species. It attacks all classes of biologic macromolecules depolymerizing polysaccharides, breaking DNA strands, inactivating enzymes, and peroxidating lipids (9 -11). NPBI is released from hemoglobin when erythrocytes are challenged by an oxidative stress (12,13). The newborn is very susceptible to NPBI-induced oxidative stress (14). Recently we reported that NPBI released by erythrocytes in vitro is much higher with hypoxic erythrocytes from newborns compared with that from adults (6). Asphyxia could affect iron metabolism and lead to a significant increase in NPBI and lipid peroxidation in plasma of newborns with hypoxic ischemic encephalopathy, indicating that iron delocalization induced by asphyxia...

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“…This results in oxidative stress in infants soon after birth (1,2). Factors such as free radical generation from oxygen exposure, inflammation, and lower antioxidant stores may result in exaggeration of this oxidative stress response.…”

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confidence: 99%

Exposure to Supplemental Oxygen and Its Effects on Oxidative Stress and Antioxidant Enzyme Activity in Term Newborn Lambs

et al. 2010

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ABSTRACT:The optimal oxygen concentration for the resuscitation of term infants remains controversial. We studied the effects of 21 versus 100% oxygen immediately after birth, and also exposure for 24 h to 100% oxygen, on oxidant lung injury and lung antioxidant enzyme (AOE) activities in term newborn lambs. Lambs at 139 d gestation were delivered and ventilated with 21% (RAR) or 100% (OXR) for 30 min. A third group of newborn lambs were ventilated with 100% O 2 for 24 h (OX24). Oxidized glutathione levels in whole blood were significantly different among the groups with lower values in the RAR group, and these values correlated highly with partial pressure of arterial oxygen (PaO 2 ). The reduced to oxidized glutathione ratio was significantly different among the groups, the ratio decreasing with increasing oxygen exposure. Lipid hydroperoxide (LPO) activity was significantly higher in the OXR and OX24 groups. AOE activity was higher in the whole lung and in red cell lysate in the OX24 group. Increased myeloperoxidase (MPO) activity, percent neutrophils, and proteins in lung lavage suggested inflammation in the OX24 group after maximal oxygen exposure. We conclude that even relatively brief exposure of the lung to 100% oxygen increases systemic oxidative stress and lung oxidant injury in ventilated term newborn lambs. (Pediatr Res 67: 66-71, 2010)

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Intraerythrocyte nonprotein-bound iron and plasma malondialdehyde in the hypoxic newborn

Cited by 87 publications

References 27 publications

Oxidative Stress in Preterm Neonates at Birth and on the Seventh Day of Life

Oxidative Stress in Preterm Neonates at Birth and on the Seventh Day of Life

Nonprotein-Bound Iron and Plasma Protein Oxidative Stress at Birth

Exposure to Supplemental Oxygen and Its Effects on Oxidative Stress and Antioxidant Enzyme Activity in Term Newborn Lambs

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