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bronchopulmonary dysplasia/glutathione
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Plasma and erythrocyte selenium and glutathione peroxidase activity in preterm infants at risk for bronchopulmonary dysplasia.
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The purpose of this study was to examine the relationships between selenium status, as measured by plasma and erythrocyte selenium and glutathione peroxidase (GPx) activity, and other postnatal factors, including selenium intake, gestational age, and oxygen dependence in preterm infants at risk for
Lower erythrocyte glutathione peroxidase activity in bronchopulmonary dysplasia in the first week of neonatal life.
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BACKGROUND
Bronchopulmonary dysplasia (BPD) is a major pulmonary complication in premature infants and is considered a free radical disorder. Erythrocyte catalase (CAT) and cellular glutathione peroxidase (c-GPx) are antioxidant enzymes that detoxify peroxides generated from dismutation of
Thioredoxin Reductase-1 Inhibition Augments Endogenous Glutathione-Dependent Antioxidant Responses in Experimental Bronchopulmonary Dysplasia.
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Association of glutathione-S-transferase-P1 (GST-P1) polymorphisms with bronchopulmonary dysplasia.
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OBJECTIVE
Reactive oxygen species (ROS) contribute to oxidative lung injury. The glutathione-S-transferases (GST) family and microsomal epoxide hydrolase (mEPHx) enzymes detoxify ROS, and genetic polymorphisms alter this detoxification. We hypothesized that polymorphisms encoding for less efficient
Employment of pulmonary superoxide dismutase, catalase, and glutathione peroxidase activity as criteria for assessing suitable animal models for studies of bronchopulmonary dysplasia.
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Selenium and glutathione peroxidase levels in premature infants in a low selenium community (Christchurch, New Zealand).
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By world standards, the selenium status of the adult population of Christchurch, New Zealand is low. To determine the status of infants undergoing neonatal intensive care, plasma and red cell selenium and glutathione peroxidase levels were measured in infants admitted to the regional neonatal unit.
Biomarkers of neutrophil-mediated glutathione and protein oxidation in tracheal aspirates from preterm infants: association with bacterial infection.
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Bronchopulmonary dysplasia is associated with neutrophil infiltration into the lungs and oxidative injury. However, the pathological importance of neutrophil oxidants is still not clear. Nosocomial pneumonia is also implicated, but the evidence is limited, in part because of the difficulty of
Glutathione synthetic activity in the lungs in newborn guinea pigs.
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Depletion of glutathione, a key antioxidant, accelerates lung injury. Glutathione concentrations are reduced significantly in premature infants with respiratory distress syndrome, leaving them at greater risk of bronchopulmonary dysplasia. A study was designed to verify if the increased glutathione
Effects of parenteral cysteine and glutathione feeding in a baboon model of severe prematurity.
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BACKGROUND
The availability of cysteine for glutathione synthesis is low in premature infants with respiratory distress.
OBJECTIVE
The effects of gestational age, oxygen delivery, and cysteine infusion or glutathione infusion, or both, on plasma total cysteine and other methionine metabolites were
[Selenium status and bronchopulmonary dysplasia in premature infants <1,500 g].
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Selenium is an essential component of the antioxidant enzyme glutathione peroxidase that protects tissues against oxidative injury by detoxifying peroxides. In preterm infants the risk for selenium deficiency is increased due to insufficient selenium uptake. Low selenium uptake and as a consequence
GSTP1 and CYP2B6 Genetic Polymorphisms and the Risk of Bronchopulmonary Dysplasia in Preterm Neonates.
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Objectives Antioxidant response plays a key role in bronchopulmonary dysplasia (BPD) pathogenesis. The glutathione-S-tranferases pi 1 (GSTP1) and cytochrome P450 (CYP) detoxification enzymes protect cells from oxidative damage. The aim of the study was to investigate whether the A313G GSTP1 and
Melatonin protects against oxidative damage in a neonatal rat model of bronchopulmonary dysplasia.
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BACKGROUND
Oxidative stress plays an important role in the pathogenesis of bronchopulmonary dysplasia (BPD). Melatonin (MT) has direct and indirect free radical detoxifying activity. The present study was to investigate whether treatment with MT would attenuate hyperoxia-induced lung injury and the
Hypoxic stress exacerbates hyperoxia-induced lung injury in a neonatal mouse model of bronchopulmonary dysplasia.
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BACKGROUND
Premature infants with lung injury often experience intermittent episodes of hypoxemia.
OBJECTIVE
This study investigates whether intermittent hypoxemia exacerbates oxidative stress and lung injury in neonatal mice in a hyperoxia-induced model of bronchopulmonary dysplasia
Ascorbylperoxide Contaminating Parenteral Nutrition Is Associated With Bronchopulmonary Dysplasia or Death in Extremely Preterm Infants.
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Ascorbylperoxide (AscOOH) is a hydrogen peroxide-dependent by-product of ascorbic acid that contaminates parenteral nutrition. In a guinea pig model, it caused oxidized redox potential, increased apoptosis, and decreased alveolarization. AscOOH detoxification is carried out by glutathione peroxidase
Antioxidative effects of caffeine in a hyperoxia-based rat model of bronchopulmonary dysplasia.
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