The suicidal death of erythrocytes should be considered a possible cause of hemolysis and plasma bilirubin overload when there is no evidence of an immune-mediated hemolytic anemia, no consumptive red blood cell disorder, no morphologic or laboratory data to suggest a problem of the red cell membrane, and no evidence of a quantitative or qualitative defect in hemoglobin synthesis.In neonatal period, xenobiotics, cytokines, osmotic shock, energy depletion, oxidative stress, and variation of temperature may induce an alteration of balance between damaging and protecting factors which can be followed by red cell death. The intraerythrocyte redox balance plays a pivotal role in orchestrating the complex molecular mechanisms leading to eryptosis.Neonatal erythrocytes are a target of extracellular free radicals and, at the same time, are themselves generators of free radicals through the Fenton reaction.This review clarifies the complex mechanisms underlying the susceptibility of neonatal erythrocytes to increased oxidative stress.

Steven Abman Anthony Absalom Thomas Abshire Wiliam Ackerman Margaret Adam Shawn K. Ahlfeld S.Faisal Ahmed Joseph L. Alcorn Eileen Steinle Alexander Omar Ali Geoffrey Ambler Istvan Arany J. Arciero Petra Clara Arck Moshe Arditi Guillaume Arlet H. Artac Stephen Ashwal Sara Aspberg Bakri Assas Chun Ting Au Renata Auricchio Richard Auten John E Baatz Tiziana Bachetti Carl Backes Praveen Ballabh Robert S. Baltimore Siddharth Banka Laura Banks Piers Barker James Barkovich Alberto Battezzati Beau Batton Olivier Baud Michel Baum Catherine Beauchemin S. Patricia Becerra Manon J. Benders Pere Berbel Anne Berg Ina bergheim Janet Elizabeth Berrington Carol Berseth Enrico Bertini Julia Beulertz Flavia Bezerra Vinod K Bhutani Marc B Bierings Stella Tracey Bjorkman Robert Black Heather Louise Blackmore Jorge Blanco Francis G Blankenberg David Bleich Joseph M. Bliss Jacky Bonaventure Avihu Boneh Riccardo Bonfanti Osvaldo Borrelli Arend F Bos Rodolfo Bracci Paolo Brambilla C Brendel Dora Brites Frank Brozovich David Elliott Brumbaugh Giacomina Brunetti Luc Bruyndonckx Karen Jane Bryson Vittoria Buccigrossi Sara Buckelew Daniel Bulte Giuseppe Buonocore David Burgner Jane C. Burns Will Bush Kara Calkins Angelo Salvatore Campanozzi Deborah Campbell Philippe Campeau Michael S. Caplan PJ Carey Waldemar A. Carlo Susan E. Carlson Virgilio P. Carnielli Marco Carotenuto David J Carr William J. Cashore Kevin A Cassady Gustavo Osvaldo Castaño Marco Castori Brian Catchpole Corrado Cecchetti Gediminas Cepinskas Lina F Chalak Wei-Chiao Chang Jennifer R Charlton Christiane Charriaut-Marlangue Raul Chavez-Valdez Fook-Choe Cheah Paul Checchia Henry Cheng Yiu Fai Cheung Terry W. Chin Valerie Y. Chock Rolando Cimaz Nevio Cimolai Tereza Cindrova-Davies Erika C. Claud Nelson Claure Pilar Codoñer-Franch Martine Cohen Solal John Connolly James Connor Giangennaro Coppola Luc Cornette Serena Counsell John M. Dagle Yun Dai Alexis S Davis Miles De Blasio Sarah D. De Ferranti Nicola De Luca Emanuella De Lucia Rolfe Linda S. de Vries Koert de Waal Charlotte Dean Justin Dean Sean Deane Roberta DeBiasi Tamas Decsi Andre Dejam Paul Delgado Olguin Christian Delles Eugene M. Dempsey Matthew Derrick Prasad Devarajan George A. Diaz Juliann DiFiore James DiNardo Lili Ding Jens Christian Djurhuus Franc C.L. Donkers Birgit Cornelia Donner Benard Dreyer Emma Gail Duerden Elia J. Duh Olivier Dulac Galit Dunietz Asim K K Duttaroy Michael B Dwinell David Eaton Danielle Ehret Barbara E Ehrlich Thomas Eiwegger Dawn Elder Maurizio Elia Nicholas Embleton Vibeke Ramsgaard Eriksen Erica A. Eugster Karen D. Fairchild Lir-Wan Fan Kathryn Noel Farrow Jia Feng Wu Rômulo Fernandes Mary S. Fewtrell Jeffrey R. Fineman Neil N. Finer I Fischbein Roslyn Holly Fitch V Flamand Brian W. Fleck Bobbi Fleiss Steven J. Fliesler Anna Forsberg P Forsythe William D. Foulkes Maria V. Fraga Mark Rohit Francis Axel Franz Mhoyra Fraser David Frommhold Richard Eugene Frye G Fueller Drude Fugelseth Ryoichi Fujiwara Camille Fung John Fuqua Sheila Gahagan Robert Galinsky Jorge Gallego Pediatr Res

Although neonatal morbidity and mortality are less than in the past, the risk of pre-natal and neonatal brain damage has not been eliminated. In order to optimize pre-natal, perinatal and neonatal care, it is necessary to detect factors responsible for brain damage and obtain information about their timing. Knowledge of the timing of asphyxia, infections and circulatory abnormalities would enable obstetricians and neonatologists to improve prevention in pre-term and full-term neonates. Cardiotocography has been criticized as being too indirect a sign of fetal condition and as having various technical pitfalls, though its reliability seems to be improved by association with pulse oximetry, fetal blood pH and electrocardiography. Neuroimaging is particularly useful to determine the timing of hypoxic-ischemic brain damage. Cranial ultrasound has been used to determine the type and evolution of brain damage. Magnetic resonance has also been used to detect antenatal, perinatal and neonatal abnormalities and timing on the basis of standardized assessment of brain maturation. Advances in the interpretation of neonatal electroencephalograms have also made this technique useful for determining the timing of brain lesions. Nucleated red blood cell count in cord blood has been recognized as an important indication of the timing of pre-natal hypoxia, and even abnormal lymphocyte and thrombocyte counts may be used to establish pre-natal asphyxia. Cord blood pH and base excess are well-known markers of fetal hypoxia, but are best combined with heart rate and blood pressure. Other markers of fetal and neonatal hypoxia useful for determining the timing of brain damage are assays of lactate and markers of oxidative stress in cord blood and neonatal blood. Cytokines in blood and amniotic fluid may indicate chorioamnionitis or post-natal infections. The determination of activin and protein S100 has also been proposed. Obstetricians and neonatologists can therefore now rely on various methods for monitoring the risk of brain damage in the antenatal and post-natal periods.

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.

Previous studies have shown that plasma lipoproteins are a common target of free radical-induced oxidative stress in hypoxic newborn infants. In contrast to lipids, the reaction of proteins with various oxidants during hypoxia has not been extensively studied. We tested the hypothesis that tissue hypoxia results in increased production of protein oxidation in cord blood of preterm newborns. Heparinized blood samples of 39 hypoxic and 16 control preterm newborns were obtained from the umbilical vein, after cord clamping immediately after delivery. Plasma levels of total hydroperoxide (TH), advanced oxidation protein products (AOPP), hypoxanthine (Hx), xanthine (Xa), and uric acid (UA) were measured. Higher Hx, Xa, UA, TH, and AOPP levels were found in hypoxic newborn infants than in controls. Statistically significant correlations were observed between: TH and Hx ( r = 0.54, p = 0.003, n = 28), AOPP and Hx ( r = 0.64, p = 0.0001, n = 27), and TH and AOPP plasma levels ( r = 0.50, p = 0.02, n = 21). In summary, TH, AOPP, Hx, Xa, and UA production is increased in fetal blood during hypoxia. The more severe the hypoxia, the higher the lipid and protein damage by free radicals.

Effects of Hypoxia on Total Hydroperoxide (TH) and Advanced Oxidation Protein Product (AOPP) in Plasma of Preterm Newborns

Effects of Hypoxia on Tyrosine Phosphorylation Pyruvate Kinase and Aconitate on Synaptosomes of Newborn Guinea Pigs

Effect of hypoxia on heat-shock proteins (HSPs) in the cerebral cortex of the guinea-pigs newborns

Hypoxia-Induced Changes in Protein Tyrosine Phosphorylation in Guinea-Pig Brain Synaptosomes 1858

Red blood cells produced by the human fetus are fundamentally different from those produced by older infants and children. They have different membrane properties, different haemoglobin, a unique metabolic profile, a much shorter life span and peculiar metabolism. The postnatal environment may cause oxidative damage to erythrocytes by enhancing the formation of toxic species of oxygen, and accelerating the normal ageing process. Newborn infant erythrocytes, especially those of premature infants, are particularly prone to oxidative damage because of limited antioxidant protective capacity, increased susceptibility to peroxidation of membrane lipids and increased ‘masked’ oxidative stress factors, such as iron status, iron-binding proteins and phagocyte activity. Red blood cells produced by the human fetus are fundamentally different from those produced by older infants and children. They have different membrane properties, different haemoglobin, a unique metabolic profile, a much shorter life span and peculiar metabolism. The postnatal environment may cause oxidative damage to erythrocytes by enhancing the formation of toxic species of oxygen, and accelerating the normal ageing process. Newborn infant erythrocytes, especially those of premature infants, are particularly prone to oxidative damage because of limited antioxidant protective capacity, increased susceptibility to peroxidation of membrane lipids and increased ‘masked’ oxidative stress factors, such as iron status, iron-binding proteins and phagocyte activity.

BACKGROUND: Polymicrogyria, a cortical abnormality usually classified among neuron migration disorders, recognizes different etiologies and pathogenetic mechanisms. In this study, a possible association between histologic chorioamnionitis and polymicrogyria was investigated.

BACKGROUND: A comprehensive knowledge of the nature and origin of amniotic fluid (AF) proteins should provide valuable information on developmental changes in fetal gene expression. In this study. AF proteins were analysed by two-dimensional electrophoresis (2-DE).

Background/Aim: Differential display of eukaryotic messengers provide means for identifying hypoxia-induced differences on gene expression in different cell types. High-resolution two-dimensional gel electrophoresis(2-D PAGE) appears to be the core technique in the study of the totality of translational products and relative post-translational processing. The aim of this study is to define developmental and hypoxia-induced variations in global protein expression in the cerebral cortical synaptosomes.