Vitamin E Attenuates the Degree of Histopathological Lung Damage Following Toluene Diisocyanate Administration in Rats

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In the current study we used a rat model of bronchial hyperreactivity induced by intranasal administration of toluene diisocyanate TDI in Wistar rats. Four experimental groups of were formed: TDI administration (TDI), control - administration of ethyl acetate (C), administration of vitamin E and TDI (TDI+E) administration of ethyl acetate and vitamin E (M+E). Our aim was to evaluate the efficiency of Vitamin E in attenuating the histopathological lesions induced by TDI in the lungs. The presence of anti-TDI IgE antibodies was demonstrated through the passive cutaneous anaphylaxis assay. Histopathological analysis of lung changes was performed by comparing the degree of peribronchiolar inflammation and goblet cell percentage between the different groups studied. Our results showed that rats sensitized to TDI presented severe inflammation of the airways, eosinophilic infiltration was present in the mid bronchi, and not limited to the central airways. Bronchial associated lymphoid tissue (BALT) hyperplasia and perivascular lymphoplasmacytic infiltrate were also identified, which is evidence of chronic inflammation of the airways. These changes were consistent with the inflammatory symptoms of bronchial hyper-reactivity observed which are similar to those in asthma patients. Vitamin E administration resulted in a statistical significant reduction in the percentage of goblet cells in the bronchial mucosa associated with a decrease inflammatory semiquantitative score, compared to the TDI group, but without statistical significance. Our data suggest that administration of vitamin E could be beneficial in attenuating the effects of TDI in individuals that develop bronchial asthma following TDI exposure.