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      Serum and Urinary Malondialdehyde (MDA), Uric acid, and Protein as markers of perinatal asphyxia

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          Abstract

          Introduction

          Perinatal asphyxia (PA) is among the leading causes of neonatal morbidity and death in neonatal intensive care units (NICUs). The aims of this research were to determine the concentrations of malondialdehyde (MDA), urine MDA, uric acid, and protein in the cord blood of neonates with perinatal asphyxia and to determine their relationship with the severity of perinatal asphyxia.

          Methods

          This matched case-control study was conducted from October 2012 to March 2013. All of the cases and controls were selected from the Gynecology & Obstetrics Department and the NICUs, at Qous Central Hospital in Qena, Egypt. We allocated 20 full-term neonates who had perinatal asphyxia to the case group. Also, we selected 20 healthy neonates for the control group. The subjects were matched with respect to age and gender. At birth and 48 hours later, measurements were made of MDA in cord blood and urine, and uric acid, protein, and creatinine also were measured in both groups. The data were analyzed by SPSS, version 17, using the independent-samples t-test, ANOVA, Tukey’s test, and Spearman’s correlation coefficient.

          Results

          At birth and 48 hr later, the newborns’ with PA had significantly higher levels of MDA in the cord blood, mean urinary uric acid/creatinine (UUA:Cr), protein/creatinine (UP:Cr), and MDA/creatinine ratio (UMDA:Cr) than the controls; their PA levels were correlated with the degree of hypoxic-ischemic encephalopathy (HIE). The babies who died due to PA had significantly higher levels of cord blood MDA, and they also had higher UUA:Cr, UP:Cr, and UMDA:Cr ratios than the babies who survived.

          Conclusion

          The concentration of MDA in cord blood can be used as a diagnostic marker of oxidative stress in asphyxiated neonates. The ratios of the urinary excretion rates of uric acid, protein, and MDA to creatinine increased as the severity of perinatal asphyxia and associated brain damage increased.

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          Most cited references19

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          Determination of free malondialdehyde in human serum by high-performance liquid chromatography.

          Lipid peroxidation involves the oxidative deterioration of polyunsaturated fatty acids in biomembranes and generates a variety of aldehydic products including malondialdehyde (MDA). To demonstrate the occurrence of lipid peroxidation in biological systems, the production of MDA has been shown to be a relevant indicator. Therefore, we describe a new method for measurement of free malondialdehyde in human serum. A simple, rapid but sensitive method for determination of MDA in human serum was applied to goiter patients and control groups. Patients with goiter had high levels of MDA compared to control groups. Our method is fast and practical for clinical measurements. The detection limit was found to be 1.2 x 10(-8) mol L(-1). Copyright 2002 Elsevier Science (USA)
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            Reperfusion injury as the mechanism of brain damage after perinatal asphyxia.

            Upon reperfusion of ischemic tissues, reactive oxygen metabolites are generated and are responsible for much of the organ damage. Experimental studies have revealed two main sources of these metabolites: 1) the oxidation of hypoxanthine to xanthine and on to uric acid by the oxidase form of xanthine oxidoreductase and 2) neutrophils accumulating in ischemic and reperfused tissue. Blocking either source will reduce reperfusion damage in a number of experimental situations. Although xanthine oxidoreductase activity may be unmeasurably low in organs other than liver and intestine, it may be involved in reperfusion injury elsewhere because of its localization in capillary endothelial cells. Time course considerations suggest that substrate accumulation and NADH inhibition of dehydrogenase activity may be more important in the pathogenesis than conversion of xanthine dehydrogenase into the oxidase form. Neutrophil accumulation may be partly due to oxidants in the first place, suggesting a link between the two sources of reactive oxygen metabolites. In the clinical context, many of the sequelae of perinatal asphyxia may be accounted for by reperfusion damage to organs such as brain, kidney, heart, liver, and lungs. During asphyxia, substrates of xanthine oxidase accumulate, upon resuscitation the cosubstrate oxygen is introduced, and evidence for oxidant production and effects has been obtained. In the pathogenesis of brain damage after asphyxia, both microvascular injury and parenchymal cell damage are important. Oxygen metabolites are involved in the former, but in the latter process their role is less clear because ischemia-reperfusion triggers not only oxidant production but many other phenomena, including gene activation, ATP depletion, glutamate accumulation, and increase of intracellular calcium. A severe insult results in cell necrosis, but more moderate asphyxia may cause delayed neuronal death through apoptosis. The time course of the changes in high energy phosphates as well as of selective neuronal death suggest that in the first hours of life there is a "therapeutic window," with future possibilities for prevention of permanent damage.
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              Long-term developmental outcome of asphyxiated term neonates.

              Asphyxia remains one of the main causes of later disability in term infants. Despite many publications identifying possible predictors of outcome in this population of interest, little is known of the long-term developmental outcome of asphyxiated term neonates. Observational studies have largely focused on short-term outcomes, with an emphasis on significant neurologic sequelae and intellectual impairments. This article reviews the literature that has described the developmental outcome of asphyxiated term newborns. As part of this review, we have also highlighted the evolution of the definition of asphyxia and delineated appropriate markers that should be used in future research on this population.
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                Author and article information

                Journal
                Electron Physician
                Electron Physician
                Electronic physician
                Electronic Physician
                Electronic physician
                2008-5842
                July 2016
                25 July 2016
                : 8
                : 7
                : 2614-2619
                Affiliations
                [1 ]Professor, Department of Pediatric, Faculty of Medicine, Minia University, Minia, Egypt
                [2 ]Assistant Professor, Department of Pediatric, Faculty of Medicine, Minia University, Minia, Egypt
                [3 ]Ph.D., Department of Pediatric, Qena Faculty of Medicine, South Valley University, Qena, Egypt
                [4 ]Lecturer, Department of Clinical and Chemical Pathology, Qena Faculty of Medicine, South Valley University, Qena, Egypt
                Author notes
                Corresponding author: Assistant Professor Dr. Sheren Esam Maher, Department of Pediatric, Faculty of Medicine, Minia University, Minia, Egypt. Tel: +20862334376, Email: Sherenesammaher@ 123456yahoo.com
                Article
                epj-08-2614
                10.19082/2614
                5014499
                96023e09-8acf-4429-beb6-40d60c71540b
                © 2016 The Authors

                This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

                History
                : 03 March 2016
                : 04 May 2016
                Categories
                Original Article

                oxidative stress,perinatal asphyxia,malondialdehyde,mda
                oxidative stress, perinatal asphyxia, malondialdehyde, mda

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