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

Buonocore, Giuseppe; Zani, S; Sargentini, I; Gioia, Dino; Signorini, Cinzia; Bracci, Rodolfo

doi:10.1111/j.1651-2227.1998.tb01390.x

Cited by 11 publications

(13 citation statements)

References 30 publications

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“…10,24 Plasma concentrations of NPBI were further increased in the HIE group when compared to controls. Such finding is consistent with a number of studies that demonstrate iron delocalization in the setting of hypoxia, 25 ischemia reperfusion 26,27 and cardiac arrest. 28 The protein-bound iron is considered a safe vehicle for iron transport and storage because it is not capable of inducing a free radical reaction.…”

Section: Discussionsupporting

confidence: 92%

Iron metabolism and lipid peroxidation products in infants with hypoxic ischemic encephalopathy

2008

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Background: Iron delocalization or misregulation of iron metabolism may play a critical role in the pathology of hypoxic ischemic encephalopathy (HIE).Objective: To study iron metabolism and lipid peroxidation in newborn infants and to correlate non-protein-bound iron (NPBI) concentration with the severity of the post-asphyxial injury and subsequent short-term outcomes.Study Design: Concentrations of NPBI and malondialdehyde (MDA) in the serum and in the cerebrospinal fluid (CSF) were measured in eight healthy newborn infants and nine newborn infants suffering from moderately severe HIE. Short-term outcomes (death, survival with or without neurological abnormality) were noted at hospital discharge.Result: Serum and CSF concentrations of both NPBI and MDA were significantly increased in HIE infants when compared to controls. Serum iron was significantly increased and total iron binding capacity was significantly decreased in HIE infants compared to controls. Out of the nine HIE infants, four infants died and two infants survived with abnormal neurological findings at hospital discharge. These six infants with clinical sequels had significantly increased concentrations of NPBI in the serum and in the CSF; and increased concentrations of MDA in the CSF when compared to the other three who survived without short-term abnormalities. Conclusion:We conclude that hypoxia ischemia alters iron metabolism and lipid peroxidation in newborn infants; and that NPBI and MDA in the CSF are increased in infants with HIE. This study supports a role for iron in oxidative injury to the central nervous system after hypoxic ischemic insults.

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Section: Discussionsupporting

confidence: 92%

Iron metabolism and lipid peroxidation products in infants with hypoxic ischemic encephalopathy

2008

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“…blood plasma in conditions of hypoxia. Additionaly, Buonocore et al (1998) reported a view that just perinatal hypoxia caused intraerythrocyte free iron release and induction of LPX in plasma of newborns. Based on these facts and our results, we assume that TBARS could be a suitable parameter of LPX extent in umbilical cord plasma of newborns.…”

Section: Discussionmentioning

confidence: 99%

Lipid peroxidation and biochemical parameters in umbilical cord blood of well-adapted term newborns

et al. 2009

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Lipid peroxidation (LPX) can play an important role in the development of pathological changes of foetal and neonatal tissues. We investigated LPX and biochemical parameters in plasma from mixed umbilical cord (m.u.c.) blood and acid-base balance (ABB) parameters in m.u.c. blood of well-adapted full-term newborns. LPX products were estimated as thiobarbituric acid reacting substances (TBARS) and were expressed by using of malondialdehyde (MDA) as a standard solution. Intensity of LPX was estimated in vitro in m.u.c. blood plasma without and with added LPX activator (125 µM L-ascorbate plus 5 µM FeSO4) and in the incubated plasma (30 min, 37• C) under both conditions. Actual TBARS (3.51 ± 0.49 nmol/mL) were determined in the non-incubated plasma without the added LPX activator. Approximately twice higher TBARS were found in the incubated plasma without the LPX activator (7.29 ± 2.17 nmol/mL) or with it (8.57 ± 2.20 nmol/mL), as well as in the non-incubated plasma after its addition (7.38 ± 1.98 nmol/mL). All analysed biochemical parameters (Fe, total iron-binding capacity, uric acid, proteins, Mg, Ca, phosphate, glucose, K, Na, Cl, ALT, AST, GMT, CK, LD, HBD, AMS, ALP, ACP) and ABB parameters were within their reference ranges. The actual TBARS levels were found being positively correlated with α-hydroxybutyrate dehydrogenase (HBD) activity and negatively with pO2. These results suggest that LPX in m.u.c. blood plasma might be activated. This activation could probably depend on extent of hypoxia. TBARS and their formation in vitro could be suitable parameters of LPX in m.u.c. blood.

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“…Recent studies reported increased intra-erythrocyte free iron levels in infants with asphyxia [41]. Iron may be released from hemoglobin in erythrocytes as result of oxidative stress [42].…”

Section: •)mentioning

confidence: 99%

Oxidative stress of the newborn in the pre‐ and postnatal period and the clinical utility of melatonin

Gitto

Pellegrino

Gitto

et al. 2009

Journal of Pineal Research

264

219

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: Newborns, and especially those delivered preterm, are probably more prone to oxidative stress than individuals later in life. Also during pregnancy, increased oxygen demand augments the rate of production of reactive oxygen species (ROS) and women, even with normal pregnancies, experience elevated oxidative stress and lipid peroxidation compared with nonpregnant women. Also, there appears to be an increase in ROS generation in the placenta of pre‐eclamptic women. In comparison with healthy adults, newborn infants have lower levels of plasma antioxidants such as vitamin E, β‐carotene, and sulphydryl groups, lower levels of plasma metal binding proteins including ceruloplasmin and transferrin, and reduced activity of erythrocyte superoxide dismutase. This review summarizes conditions of newborns where there is elevated oxidative stress. Included in this group of conditions is asphyxia, respiratory distress syndrome and sepsis and the review also summarizes the literature related to clinical trials of antioxidant therapies and of melatonin, a highly effective antioxidant and free radical scavenger. The authors document there is general agreement that short‐term melatonin therapy may be highly effective and that it has a remarkably benign safety profile, even when neonates are treated with pharmacological doses. Significant complications with long‐term melatonin therapy in children and adults also have not been reported. None of the animal studies of maternal melatonin treatment or in postnatal life have shown any treatment‐related side effects. The authors conclude that treatment with melatonin might result in a wide range of health benefits, improved quality of life and reduced healthcare costs and may help reduce complications in the neonatal period.

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

Cited by 11 publications

References 30 publications

Iron metabolism and lipid peroxidation products in infants with hypoxic ischemic encephalopathy

Iron metabolism and lipid peroxidation products in infants with hypoxic ischemic encephalopathy

Lipid peroxidation and biochemical parameters in umbilical cord blood of well-adapted term newborns

Oxidative stress of the newborn in the pre‐ and postnatal period and the clinical utility of melatonin

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