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Neonatal Selenium Deficiency Decreases Selenoproteins in the Lung and Impairs Pulmonary Alveolar Development
Laura G Sherlock1, William C McCarthy1, Maya R Grayck1
1Perinatal Research Center, Department of Pediatrics, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA.
Insights
Maternal selenium deficiency during pregnancy and lactation impairs neonatal lung growth and development. This study identifies key selenoproteins affected, impacting antioxidant defenses and cell signaling in offspring.
Area of Science:
- Biochemistry
- Developmental Biology
- Nutritional Science
Background:
- Low selenium levels in children are linked to poor respiratory health.
- Selenium is crucial for antioxidant enzymes and proteins.
- The impact of maternal selenium deficiency on neonatal lung development is not well understood.
Purpose of the Study:
- To investigate how maternal selenium deficiency during pregnancy and lactation affects neonatal pulmonary selenoproteins, growth, and lung development.
- To identify specific selenoproteins in the neonatal lung that are reduced by selenium deficiency.
Main Methods:
- A neonatal selenium deficiency model was used, limiting selenium intake in dams during pregnancy and lactation.
- Neonatal pulmonary selenoprotein levels and lung development were assessed at postnatal days 0 and 7.
- Activity and protein content of key enzymes like glutathione peroxidase (GPx) and thioredoxin reductase (Txnrd) were measured.
Main Results:
- Selenium-deficient pups showed reduced weight and impaired alveolar development compared to controls.
- Activity of GPx and Txnrd, and protein levels of GPx1, GPx3, and Txnrd1 were decreased in selenium-deficient lungs.
- Selenoprotein N, important for alveolar development, was reduced in selenium-deficient neonatal lungs.
Conclusions:
- Maternal selenium deficiency during gestation and lactation negatively impacts offspring weight gain and lung growth.
- Several neonatal lung selenoproteins are sensitive to reduced selenium intake, potentially affecting oxidative stress and signaling pathways.
Abstract:
Decreased selenium (Se) levels during childhood and infancy are associated with worse respiratory health. Se is biologically active after incorporation into Se-containing antioxidant enzymes (AOE) and proteins. It is unknown how decreased maternal Se during pregnancy and lactation impacts neonatal pulmonary selenoproteins, growth, and lung development. Using a model of neonatal Se deficiency that limits Se intake to the dam during pregnancy and lactation, we evaluated which neonatal pulmonary selenoproteins are decreased in both the saccular (postnatal day 0, P0) and early alveolar (postnatal day 7, P7) stages of lung development. We found that Se deficient (SeD) pups weigh less and exhibit impaired alveolar development compared to Se sufficient (SeS) pups at P7. The activity levels of glutathione peroxidase (GPx) and thioredoxin reductase (Txnrd) were decreased at P0 and P7 in SeD lungs compared to SeS lungs. Protein content of GPx1, GPx3 and Txnrd1 were decreased in SeD lungs at P0 and P7, whereas Txnrd2 content was unaltered compared to SeS controls. The expression of NRF-2 dependent genes and several non-Se containing AOE were similar between SeS and SeD lungs. SeD lungs exhibited a decrease in selenoprotein N, an endoplasmic reticulum protein implicated in alveolar development, at both time points. We conclude that exposure to Se deficiency during pregnancy and lactation impairs weight gain and lung growth in offspring. Our data identify multiple selenoproteins in the neonatal lung that are vulnerable to decreased Se intake, which may impact oxidative stress and cell signaling under physiologic conditions as well as after oxidative stressors.
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