Characteristics and Functional Properties of Red Cells during the First Days of Life

Buonocore, Giuseppe; Berni, Silvia; Gioia, Dino; Bracci, Rodolfo

doi:10.1159/000243399

Cited by 10 publications

(4 citation statements)

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“…This peculiarity of neonatal red cells has been proposed as potentially responsible for anaemia in preterm infants (9). Recent observations suggest that oxidative stress plays a role in the slight rheological abnormalities observed in the first hours of life (8) and in neonatal hyperbilirubinaemia (10). Research into the mechanisms of intracellular release of highly reactive molecules capable of inducing erythrocyte injury has shown that the first stages of oxidative red cell damage can be detected by evaluating the intra-erythrocyte free iron concentration (IFIC) (11).…”

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confidence: 98%

“…Investigations carried out in the last few years have demonstrated that newborn red cells exposed to oxidizing agents show increased membrane lipid peroxidation, increased Heinz body formation, high methaemoglobin content and increased content of haemoglobin oxidation products (1)(2)(3)(4)(5)(6). Although detailed information is available on the increased susceptibility of neonatal erythrocytes exposed ''in vitro'' to oxidizing agents (1)(2)(3)(4)(5)(6)(7)(8)(9), the true extent of oxygen toxicity to red cells ''in vivo'' is still uncertain. This peculiarity of neonatal red cells has been proposed as potentially responsible for anaemia in preterm infants (9).…”

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confidence: 99%

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Hypoxia‐induced free iron release in the red cells of newborn infants*

et al. 1998

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Heparinized blood samples were obtained at birth from 164 newborn infants (101 full term; 63 preterm). Intra‐erythrocyte free iron concentration and hypoxanthine plasma levels were determined by high‐pressure liquid chromatography. Intra‐erythrocyte free iron concentration was higher in preterm than in full term babies (p < 0:0001) and adults (p < 0:0001). Statistically significant correlations were observed between intra‐erythrocyte free iron concentration and hypoxanthine levels (r = 0:66; p= 0:0001), pH (r = ‐ 0:76; p = 0:0001), base excess (r = ‐ 0:79; p= 0:0001), and gestational age (r = ‐ 0:44; p= 0:0001) in both infant populations. Multiple regression analysis between intra‐erythrocyte free iron concentration in cord blood, as an independent variable, and Apgar score at 1 min, pH, base excess, hypoxanthine values, FiO2 needed for resuscitation immediately after delivery, and gestational age, as dependent variables, identified hypoxanthine levels (p= 0:0003; partial F‐test = 15.4) as the best single predictor of intra‐erythrocyte free iron concentration. In conclusion, hypoxia induces intra‐erythrocyte free iron release, and therefore enhances the risk of oxidative injury due to hydroxyl radical generation.

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confidence: 98%

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Hypoxia‐induced free iron release in the red cells of newborn infants*

et al. 1998

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“…Red cell deformation is wider in the fetus and neonates than in adults, and more variable, with populations of more highly deformable, but also more poorly deformable, erythrocytes (44). The red cell ltration rate of preterm and term infants is not signi cantly different from that of adults; however, it appears to decrease in the rst hours of life, in parallel with the increase in density (45).…”

Section: Oxidative Injury Of the Neonatal Red Cellmentioning

confidence: 99%

Oxidant injury in neonatal erythrocytes during the perinatal period

2002

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It has been known for many decades that oxidative stress leads to oxidation of hemoglobin and damage to the erythrocyte membrane. More recently, the factors involved in denaturating of membrane proteins and lipid peroxidation have been investigated in detail, as well as the mechanism of reactive oxygen species formation in red cells. Oxidative stress depletes adenosine triphosphate (ATP) and adenine nucleotides, whereas adenosine monophosphate (AMP) deaminase seems to depress energy metabolism by blocking the salvage pathway of purine nucleotides. Depletion of ATP and activation of AMP deaminase are related to calcium ion concentrations. Denaturating of membrane proteins generally precedes lipid peroxidation and consequent phagocytosis due to caspase activation. Extensive investigations demonstrated the key role of oxidative stress and iron release in a reactive form causing membrane protein damage via the Fenton reaction and hydroxyl radical production. In the absence of efficient protection by antioxidant factors and other molecules such as flavonoids, oxidative stress is responsible for the release of iron in reactive form, predisposing red cells to hemolysis through the formation of senescence antigen. Other well‐known sources of oxidative stress in red cells are free radical production outside the red cell by activated phagocytes, endothelial metabolism, hyperoxia, ischemia‐reperfusion and the arachidonic acid cascade. Conclusion: The recent insight into the mechanism of oxidative injury of red cells and evidence of relationships between erythrocyte oxidative stress and hypoxia suggest that increased hemolysis is induced by severe hypoxia and acidosis in the fetus as well as the newborn.

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“…On days 2-4 of life, we found relatively high values of intracellular GSHPx activity compared to the results of several cord blood studies. Buonocore et al have also described significant elevation of RBC GSHPx activity simultaneously with RBC oxidative injury by day 4 of life (7).…”

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confidence: 94%