Lung injury induced by Bisphenol A: A food contaminant, is ameliorated by selenium supplementation

Bisphenol A (BPA), a widely used industrial chemical, is known to disrupt endocrine function. This study aimed to investigate the impact of chronic exposure to BPA on the lung tissue of adult male rats as well as any possible alleviating effects resulting from selenium (Se) treatment. Chronic exposure to BPA resulted in prominent inflammation and oxidative stress responses as evidenced by an increase in levels of malondialdehyde (MDA), reduced concentrations of superoxide dismutase (SOD), and upregulation of Interleukin-18 (IL-18) expression in lung tissue. In addition, chronic exposure led to modulation of the fibrosis-related gene expression, as we observed augmented follistatin-like1 (FSTL1) expression and diminished a disintegrin and metalloproteinase with thrombospondin motif 5 (ADAMTS5) expression. Se treatment remarkably mitigated changes in the expression of these dysregulated markers of lung injury. The biochemical changes were consistent with the histopathological findings, where cellular infiltration and inflammatory fibrotic changes were observed following BPA administration and a lessening of these effects with concomitant Se treatment. Taken together, the results from the study reveal that chronic exposure to BPA may promote the development of pulmonary inflammatory diseases with possible induction of lung fibrosis. Se treatment effectively suppressed oxidative stress, inflammation, and fibrosis, suggesting that Se has the potential to be used as a therapeutic agent in the treatment of pulmonary inflammatory diseases.