A novel approach to study oxidative stress in neonatal respiratory distress syndrome

Negi, Reena; Pande, Deepti; Karki, Kanchan; Kumar, Ashok; Khanna, Ranjana S.; Khanna, Hari D.

doi:10.1016/j.bbacli.2014.12.001

Cited by 32 publications

(38 citation statements)

References 31 publications

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“…4 ROS can cause damage to a variety of cellular molecules, including lipids, proteins, and DNA, which results in cell injury and may induce respiratory cell death. 5,6 ROS also interact with pulmonary surfactant, thus delaying the normal functioning of the lung. 5 This process can contribute to the pathogenesis of RDS and very likely leads to severe RDS.…”

Section: Introductionmentioning

confidence: 99%

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Oxidative stress markers in neonatal respiratory distress syndrome: advanced oxidation protein products and 8-hydroxy-2-deoxyguanosine in relation to disease severity

et al. 2019

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We assessed oxidant-antioxidant status and evaluated the role of lipid peroxidation, oxidative DNA damage, and protein oxidation in the development and severity of neonatal respiratory distress syndrome (RDS). METHODS: Forty preterm neonates with RDS were compared with another 40 preterm neonates without RDS enrolled as controls. Total antioxidant capacity (TAC), malondialdehyde (MDA), advanced oxidation protein products (AOPPs), 8-hydroxy-2deoxyguanosine (8-OHdG), and trace elements (copper and zinc) were measured in cord blood (day 0) for all neonates and repeated on day 3 for the RDS group. RESULTS: Day 0 serum levels of MDA, AOPPs, and 8-OHdG were significantly higher in neonates with RDS than controls with a further increase on day 3. Days 0 and 3 levels of TAC, copper, and zinc were significantly lower in the RDS group compared with controls. Elevated serum levels of 8-OHdG and AOPPs were associated with severe RDS, invasive mechanical ventilation, and high mortality rate. 8-OHdG and AOPPs were positively correlated with MDA, oxygenation index, duration of ventilation, and duration of hospitalization. CONCLUSIONS: Increased lipid, protein, and DNA oxidation is accompanied by alterations in the antioxidant defense status, which may play a role in the pathogenesis and severity of RDS.

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Section: Introductionmentioning

confidence: 99%

“…5,6 ROS also interact with pulmonary surfactant, thus delaying the normal functioning of the lung. 5 This process can contribute to the pathogenesis of RDS and very likely leads to severe RDS. 7 ROS have been implicated in the molecular damage seen in the bronchoalveolar lavage (BAL) fluid of patients with RDS.…”

Section: Introductionmentioning

confidence: 99%

Oxidative stress markers in neonatal respiratory distress syndrome: advanced oxidation protein products and 8-hydroxy-2-deoxyguanosine in relation to disease severity

et al. 2019

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“…A number of studies have demonstrated that the association of melatonin with misoprostol, a gastric mucosal protective agent, is more beneficial than melatonin therapy alone. These studies on animals found that the administration of 10 mg/kg body weight melatonin for 3 days to animals with induced NEC-like lesions significantly reduced the severity of the disease by decreasing cytokine levels and stimulating antioxidant enzyme activity [45,48].…”

Section: Effects Of Oxidative Stress In Ulceronecrotic Enterocolitismentioning

confidence: 99%

“…Caspase 6 and, subsequently, caspase 3 are activated. NMDA receptor activation depresses the mitochondrial respiratory process and induces apoptosis-a process which is not found in adults, known as the NMDA paradox [41,48].…”

Section: Effects Of Oxidative Stress In Neonatal Asphyxia and Hypoxicmentioning

confidence: 99%

Particularities of Oxidative Stress in Newborns

Matyas¹,

Zaharie²

2018

Novel Prospects in Oxidative and Nitrosative Stress

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The oxidative stress at newborns is augmented by different conditions like preterm birth, asphyxia, respiratory distress, and intraventricular hemorrhage. Preterm neonates associate a more pronounced oxidative stress than healthy term newborns. Several neonatal conditions like respiratory distress (RDS), asphyxia, intraventricular hemorrhage, bronchopulmonary dysplasia, retinopathy, and necrotizing enterocolitis will increase the oxidative stress. The harmful effects of free radicals are linked to their capacity to react with polyunsaturated fatty acids of cell membranes, proteins, and nucleic acids. Free radicals will produce protein alteration with function loss and lipid peroxidation.

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“…Elevations of urinary leukotriene E 4 have been associated with ARDS in adults ( 173 ) and development of BPD in infants ( 174 , 175 ), though variations observed may be highly affected by gestational age and maturity ( 176 ). Several studies of neonates have demonstrated alterations in the levels of markers of oxidative stress and DNA damage in RDS ( 175 , 177 ), and one study of BAL fluid in children with ALI found alterations in the concentrations of multiple cell surface lipids indicative of alveolar–capillary membrane damage ( 21 ). Eicosanoids and other lipid-derived and small molecules may serve as useful biomarkers, especially of vascular physiology, oxidative damage, and inflammation, in future studies of children with ARDS.…”

Section: Biomarker Subgroupsmentioning

confidence: 99%

Biomarkers in Pediatric ARDS: Future Directions

Orwoll

Sapru

2016

Front. Pediatr.

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Acute respiratory distress syndrome (ARDS) is common among mechanically ventilated children and accompanies up to 30% of all pediatric intensive care unit deaths. Though ARDS diagnosis is based on clinical criteria, biological markers of acute lung damage have been extensively studied in adults and children. Biomarkers of inflammation, alveolar epithelial and capillary endothelial disruption, disordered coagulation, and associated derangements measured in the circulation and other body fluids, such as bronchoalveolar lavage, have improved our understanding of pathobiology of ARDS. The biochemical signature of ARDS has been increasingly well described in adult populations, and this has led to the identification of molecular phenotypes to augment clinical classifications. However, there is a paucity of data from pediatric ARDS (pARDS) patients. Biomarkers and molecular phenotypes have the potential to identify patients at high risk of poor outcomes, and perhaps inform the development of targeted therapies for specific groups of patients. Additionally, because of the lower incidence of and mortality from ARDS in pediatric patients relative to adults and lack of robust clinical predictors of outcome, there is an ongoing interest in biological markers as surrogate outcome measures. The recent definition of pARDS provides additional impetus for the measurement of established and novel biomarkers in future pediatric studies in order to further characterize this disease process. This chapter will review the currently available literature and discuss potential future directions for investigation into biomarkers in ARDS among children.

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A novel approach to study oxidative stress in neonatal respiratory distress syndrome

Cited by 32 publications

References 31 publications

Oxidative stress markers in neonatal respiratory distress syndrome: advanced oxidation protein products and 8-hydroxy-2-deoxyguanosine in relation to disease severity

Oxidative stress markers in neonatal respiratory distress syndrome: advanced oxidation protein products and 8-hydroxy-2-deoxyguanosine in relation to disease severity

Particularities of Oxidative Stress in Newborns

Biomarkers in Pediatric ARDS: Future Directions

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