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Histological and biochemical studies on the effect of vitamin E on sodium fluoride induced lung toxicity in adult albino rats

Introduction Fluoride compounds are naturally present in soil, water, and food. Furthermore, fluoride in amounts exceeding the standard therapeutic dosage accumulates in hard and soft tissues, where it disturbs the metabolic processes and produces noticeable changes in multiple organs. Aim The study was designed to investigate the effects of sodium fluoride (NaF) on the lung of adult albino rats and the possible protective role of vitamin E on these changes. Materials and methods Twenty-six adult albino rats were divided into three groups: group I (control), group II receiving NaF alone (10 mg/kg body weight), and group III receiving the same NaF dose together with vitamin E supplementation (3 mg/day orally for 35 days). Tissue homogenates were collected for biochemical study, and the lung tissues were excised for histological, immunohistochemical, and biochemical studies. The results of biochemical and immunohistochemical studies were measured and statistically analyzed. Results Lung sections of rats treated with NaF showed congestion and injury in the endothelium of blood vessels, with hemorrhage and injury in the alveolar epithelium. Proliferation of pneumocytes type II and interstitial septal cells were seen. Thickening of interalveolar septum by cellular infiltration and red blood cells with subsequent decrease in the alveolar space was observed. Some area showed compensatory dilated alveolar ducts. A significant increase in the mean area% of cyclooxygenase-2-immunopositive cells was observed when compared with other groups. There was a significant decrease in the catalase activity and an increase in malondialdehyde concentration in group II. In vitamin E-treated group, most fields showed normal lung structure and some fields showed thickened interalveolar septa and dilated air spaces. Conclusion The use of vitamin E has a beneficial effect on the protection of lung against NaF-induced injury.