Potential Protective Role of Vitamin E in Lung of Adult Male Albino Rat Exposed to Bisphenol A

Abstract Background: Bisphenol A (BPA) is a worldwide manu-factured chemical in plastic industry. Exposure to BPA through food and drinking water in plastic containers leads to human health problems. Aim of Study: This study intends to explore the possible protective role of vitamin E against BPA induced functional and structural changes in the lungs of adult male albino rats. Material and Method: Twenty four adult male albino rats were divided randomly into 4 equal groups of 6 rats each; Group I (controls) divided into 2 subgroups: Subgroup (A) (negative control group): Fed on regular diet and water for 8 weeks. Subgroup (B) (vehicle control group): Received (1ml of corn oil) by oral gavage/day for 8 weeks. Group II (vitamin E alone) received 200mg Vitamin E/kg/day; Group III (BPA alone) received 500mg BPA/kg/day; Group IV (BPA and vitamin E co-administered) as in groups II and III. The drugs were administered through oral gavage for 8 weeks, at the end of the experiment, heart rate (HR) and mean arterial blood pressure (MABP) were estimated for all the animals. Blood samples were withdrawn for chemical examinations, and after sacrifice fresh lung specimens were collected for histological examination. Results: Administration of Vitamin E in cooperation with BPA significantly decreased MDA levels, MPO and Caspase-3 activities. In addition, it increased GSH, CAT and SOD activities significantly in rat lung tissues. Also, plasma levels of TNF-a, IL-1b, IL-6 and LDH were significantly decreased. Blood gases analysis showed no significant difference in pH, but showed increase in PaO2 decrease in PaCO2 significantly. Moreover hemodynamics changes in the form of significant decrease in MABP and HR. Vitamin E protected lungs against BPA induced histopathological changes like inflammation, congestion, inter alveolar septum thickening, alveolar damage, collagen fibers percent area and fatty infiltration, also the immunohistochemical changes were altered as depicted by significant decrease in the cluster of differentiation 68 (CD68) +ve cell count and decreased expression of nuclear factor kappa B (NF-kB) in immunestained cells of the lung tissue.
Conclusion: BPA exposure induced oxidative stress, inflammation and structural lung injury which were signifi-cantly less by coadminstration of vitamin E supplementation.