bronchopulmonary dysplasia/glutatión

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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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Aurothioglucose- (ATG-) mediated inhibition of thioredoxin reductase-1 (TXNRD1) improves alveolarization in experimental murine bronchopulmonary dysplasia (BPD). Glutathione (GSH) mediates susceptibility to neonatal and adult oxidative lung injury. We have previously shown that ATG

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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While additional oxygen supply is often required for the survival of very premature infants in intensive care, this also brings an increasing risk of progressive lung diseases and poor long-term lung outcomes. Caffeine is administered to neonates in neonatal intensive care for the

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