Evaluation of lung toxicity in rats kept in coal mine ambience by in vivo respiration records: An Experimental Study

OBJECTIVE: Mine workers exposed to dusts or toxic gasses in occupational atmospheric conditions. Pneumoconiosis and other lung diseases are charecterized by the pathogenesis of coal dust-caused pulmonary toxicity associated with reactive oxygen species (ROS). MATERIALS AND METHODS: This study was conducted to investigate the respiration failures and fibrosis in rats after being exposed to coal dust and gases in mine atmosphere. Another aim was to study the therapeutic effect of erdosteine as antioxidant therapy. Rats were exposed to mine ambience for four week, and then they were breathed in the clean air for four week. The respiratory functions of rats were recorded once a week for eight week, as in vivo. The fibrosis of lung tissue levels, the oxidant/antioxidant status, and cytokines of inflammation in bronchoalveolar lavage fluids (BALFs) were evaluated, at the end of the processes. RESULTS: We observed to be the beginning of respiratory abnormalities in animals exposed to coal dust in second week. The end of fourth week, there were the increase of respiratory frequency and along with the decrease of respiratory depth. The respiratory failures were not improved in clean ambience, moreover apnea were appearance in the end of six week (the second week of clean air). Deaths were 28% in animals. Erdosteine administer to rats could not fully abolished to the pulmonary toxicity, however could able to hold to toxicity, and also there were not dies in rats administered to erdosteine. Coal dust exposure was resulted in fibrosis with higher hydroxyproline (HP) levels, cytokine inflammation with higher interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) levels, and lipid peroxidation with an increased malondialdehyde (MDA) levels, according to the healthy. A dramatically run out of endogen antidote sulfide pools (GSH), and an increased MPO activity were dedected in the mine dusts and gasses exposure group, according to the healthy animals. High biochemical index of toxicity were partly balanced by erdosteine. CONCLUSIONS: Our experimental findings support the hypothesis that ROS is induced coal workers' pneumoconiosis. Re-oxygenation cannot be getting it together to reverse the pulmonary toxicity. On the top of it, it can make its pathogenesis further exaggerating and even worse. On this account we heartily speculate that re-oxygenation should be by steps in mine workers. In addition the antioxidant therapy may be partly a choice be able to tolerate the coal dust-induced lung toxicity of mine workers