Selenium deficiency modulates neonatal pulmonary alveolar development via mitochondrial ROS accumulation and oxidative stress mediated by STAT3 inhibition.

Abstract

Context: Recent findings suggest that Selenium (Se) deficiency in neonates may hinder pulmonary alveolar development, but the underlying molecular mechanisms remain underexplored.

Objective: This study utilised a neonatal mouse model to investigate the effects of dietary Se deficiency on pulmonary alveolar development.

Materials and methods: Techniques such as quantitative PCR, Western blotting, and immunohistochemistry were employed to assess gene and protein expression related to alveolar development and oxidative stress markers. Mitochondrial ROS accumulation was quantified using MitoSOX staining, and the activity of sirtuin 3 (STAT3), a key transcription factor involved in oxidative stress responses, was analysed.

Results: Our findings indicate that Se-deficient neonates exhibit significantly impaired alveolar development characterised by reduced alveolar number and surface area. These structural alterations were associated with increased mitochondrial ROS levels and oxidative stress. Furthermore, Se deficiency resulted in decreased STAT3 phosphorylation, suggesting a mechanism whereby Se influences alveolar development through modulation of STAT3 activity and mitochondrial function.

Discussion and conclusion: Se plays a critical role in neonatal pulmonary development by modulating oxidative stress and mitochondrial dynamics via the STAT3 pathway. The study underscores the potential of Se supplementation as a strategic intervention to promote alveolar maturation and prevent pulmonary disorders in neonates. Further research is recommended to explore the therapeutic thresholds and timing of Se administration to optimize pulmonary outcomes.