Abstract

Abstract Background: Cyclosporine A (Cs A) is an immunosup-pressive agent which used in treatment of various autoimmune diseases. Aim of Study: Evaluation of the effect of cyclosporin-A administration on the histological structure on the lung in adult male rat and the protective role of vitamin E. Material and Methods: Forty adult male albino rats were divided equally into four groups. Group 1 received distilled water, Group 2 received oral daily dose of cyclosporine A (10mg/kg/body weight) for 4 weeks, Group 3 (a co-treated group) received oral daily dose of vitamin E (200mg/kg/body weight) simultaneously with cyclosporine A (10mg/kg/body weight) for 4 weeks, and Group 4 (a pre-treated group) received oral daily dose of vitamin E (200mg/kg) 2 hours prior to treatment with cyclosporine A (10mg/kg body weight) for 4 weeks. Lung specimens were taken out and processed for histopathological examination and for assessment of lung tissue levels of oxidative stress markers (MDA, SOD, GSH, and CAT). Results: Histopathological examination using light and electron microscope revealed that cyclosporine-A induced deleterious histopathological changes in the lungs of adult male albino rats. Focal destruction of alveolar walls, formation of emphysematous air spaces, distortion of the interalveolar septa, peri-bronchial inflammatory cell infiltration and con-gestion with fibrosis. Pneumocytes type I showed an irregular nucleus. Pneumocytes type II revealed irregular pyknotic nuclei, numerous vacuolated or empty lamellar bodies with loss of their lamellar arrangement, and distorted surface microvilli. There was significant increase in lung malondial-dehyde (MDA) level, with significant decrease in lung super-oxide dismutase (SOD), glutathione peroxidase (GSH), and catalase (CAT). Vitamin E either with or before receiving cyclosporin-A reduced lung affection with improved level of oxidative markers in the lung homogenates. Conclusion: Vitamin E reduced cyclosporin-A lung affec-tion with improved level of oxidative markers in the lung homogenates.

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