Oxidative stress diseases unique to the perinatal period: A window into the developing innate immune response

Dietz, Robert M.; Wright, Clyde J.

doi:10.1111/aji.12787

Cited by 11 publications

(13 citation statements)

References 148 publications

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“…TLR3 activation hinders neural progenitor cell proliferation during brain maturation, and the inhibition of TLR-3 in fetal life modifies brain development through IL-6 signaling. TLR-1, -2, and -7 are upregulated 24 h after any injury, and TLR-2, -3, -6, -7, and -9 are upregulated 72 h after hypoxic-ischemic injury; meanwhile, TLR-5 is downregulated in the first 24 h [64].…”

Section: Melatonin and Brain Injurymentioning

confidence: 94%

Use of Melatonin in Oxidative Stress Related Neonatal Diseases

et al. 2020

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Reactive oxygen species have a crucial role in the pathogenesis of perinatal diseases. Exposure to inflammation, infections, or high oxygen concentrations is frequent in preterm infants, who have high free iron levels that enhance toxic radical generation and diminish antioxidant defense. The peculiar susceptibility of newborns to oxidative stress supports the prophylactic use of melatonin in preventing or decreasing oxidative stress-mediated diseases. Melatonin, an effective direct free-radical scavenger, easily diffuses through biological membranes and exerts pleiotropic activity everywhere. Multiple investigations have assessed the effectiveness of melatonin to reduce the “oxygen radical diseases of newborn” including perinatal brain injury, sepsis, chronic lung disease (CLD), and necrotizing enterocolitis (NEC). Further studies are still awaited to test melatonin activity during perinatal period.

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Section: Melatonin and Brain Injurymentioning

confidence: 94%

Use of Melatonin in Oxidative Stress Related Neonatal Diseases

et al. 2020

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“…Our findings demonstrate that insufficient Se supply in the perinatal period results in decreased circulating GPx as well as hepatic GPx and eventually Trxrd1. As infants can experience a myriad of oxidative challenges, insufficient selenoenzyme defense may increase neonatal morbidities or mortality [ 17 ]. Neonatal Se levels are not routinely measured as standard of care [ 41 ].…”

Section: Discussionmentioning

confidence: 99%

“…Se is a trace mineral essential for redox homeostasis and response to oxidative stress [ 12 , 13 ]. An impaired ability to respond to oxidative challenges is associated with morbidity and mortality in the neonatal period, and it is possible that decreased Se-associated antioxidant enzymes (AOE) may contribute to disrupted organogenesis and injury during infancy [ 14 , 15 , 16 , 17 ]. However, Se deficiency can occur concordantly with poor overall nutrition [ 18 ].…”

Section: Introductionmentioning

confidence: 99%

Neonatal Selenoenzyme Expression Is Variably Susceptible to Duration of Maternal Selenium Deficiency

et al. 2021

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Maternal selenium (Se) deficiency is associated with decreased neonatal Se levels, which increases the risk for neonatal morbidities. There is a hierarchy to selenoprotein expression after Se deficiency in adult rodents, depending on the particular protein and organ evaluated. However, it is unknown how limited Se supply during pregnancy impacts neonatal selenoprotein expression. We used an Se-deficient diet to induce perinatal Se deficiency (SeD), initiated 2–4 weeks before onset of breeding and continuing through gestation. Neonatal plasma, liver, heart, kidney, and lung were collected on the day of birth and assessed for selenoproteins, factors required for Se processing, and non-Se containing antioxidant enzymes (AOE). Maternal SeD reduced neonatal circulating and hepatic glutathione peroxidase (GPx) activity, as well as hepatic expression of Gpx1 and selenophosphate synthetase 2 (Sps2). In contrast, the impact of maternal SeD on hepatic thioredoxin reductase 1, hepatic non-Se containing AOEs, as well as cardiac, renal, and pulmonary GPx activity, varied based on duration of maternal exposure to SeD diet. We conclude that the neonatal liver and circulation demonstrate earlier depletion in selenoenzyme activity after maternal SeD. Our data indicate that prolonged maternal SeD may escalate risk to the neonate by progressively diminishing Se-containing AOE across multiple organs.

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“…It has been reported that lung injury may be associated with ROS [12,13]. It is known that NF-κBp65, which plays an important role in immune response, inflammatory response and apoptosis, is a transcription factor widely distributed in a variety of cells [14]. It usually binds to the inhibitor I B to form an inactive cytoplasmic heterodimer.…”

Section: Discussionmentioning

confidence: 99%

Expression levels of reactive oxygen species, NF-κBp65 and TGF-β1 and their correlations in bronchopulmonary dysplasia in neonatal rats

Wang¹,

Sun²,

Wang³

et al. 2020

Trop. J. Pharm Res

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Purpose: To study the levels of reactive oxygen species (ROS), nuclear transcription factor-κBp65 (NF-κBp65) and TGF-1, and their correlation in bronchopulmonary dysplasia in neonatal rats.Methods: Twenty (20) pregnant rats were randomly divided into study and normal groups. Radial alveolar counts were carried out at 2, 8 and 15 days of age. The levels of ROS expression in the lung tissues of the two groups were assayed by ELISA while immunohistochemistry was used to determine the expressions of TGF-β1 and NF-κBp65 in neonatal lung tissues of the two groups. Pearson correlation test was used to analyze correlations amongst ROS, TGF-β1 and NF-κBp65 in the neonatal lung tissues.Results: At days 8 and 9 after birth, radial alveolar count was significantly lower in study rats than in control rats (p < 0.05). Expression levels of ROS, TGF-β1 and NF-κBp65 in study group were markedly raised at days 2, 4 and 8 after birth, relative to control (p < 0.05).Conclusion: The levels of ROS, TGF-β1 and NF-κBp65 in bronchopulmonary dysplasia in neonatal rats are significantly and positively correlated, and are higher than those in normal rats. This provides a scientific basis for development of drugs for bronchopulmonary dysplasia. Keywords: Neonatal rats, Bronchopulmonary dysplasia, Lung tissue, NF-κBp65, TGF-β1, Correlation

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Oxidative stress diseases unique to the perinatal period: A window into the developing innate immune response

Cited by 11 publications

References 148 publications

Use of Melatonin in Oxidative Stress Related Neonatal Diseases

Use of Melatonin in Oxidative Stress Related Neonatal Diseases

Neonatal Selenoenzyme Expression Is Variably Susceptible to Duration of Maternal Selenium Deficiency

Expression levels of reactive oxygen species, NF-κBp65 and TGF-β1 and their correlations in bronchopulmonary dysplasia in neonatal rats

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