Toxic effects of inhaled sulfur mustard (SM) on the histology of visceral organs was investigaed by exposing mice to 84. 6mg/m3 for 1h duration, using controlled single exposure conditions. A progressive fall in body...Toxic effects of inhaled sulfur mustard (SM) on the histology of visceral organs was investigaed by exposing mice to 84. 6mg/m3 for 1h duration, using controlled single exposure conditions. A progressive fall in body weight from third day onwards was noticed. Light microscopic examination of the pulmonary tissue of these animals at 6 h post exposure revealed that the tracheobronchial epithelium remained intact, but was infiltrated by inflammatory cells. By 24 h post exposure, the mucosecretory cells were destroyed. The indanunatory reaction was maximum at 48 h. By 7th day post exposure there was swelling and vacuolation of lung parenchymal cells and thrombi formation. In addition SM caused congestion and hemorrhage at alveolar level. SM also caused granulovacuolar degeneration with perinuclear clumping of the cytopasm of hepatocytes and renal parenchymal cells. Renallesions were chazacterized by congestion and hemorrhage. Among visceral tissues, maximum atrophywas observed in spleen. Distribution of lesions increased with post exposure period. The maximum lesions were observed at 7th day post-exposure.展开更多
文摘Toxic effects of inhaled sulfur mustard (SM) on the histology of visceral organs was investigaed by exposing mice to 84. 6mg/m3 for 1h duration, using controlled single exposure conditions. A progressive fall in body weight from third day onwards was noticed. Light microscopic examination of the pulmonary tissue of these animals at 6 h post exposure revealed that the tracheobronchial epithelium remained intact, but was infiltrated by inflammatory cells. By 24 h post exposure, the mucosecretory cells were destroyed. The indanunatory reaction was maximum at 48 h. By 7th day post exposure there was swelling and vacuolation of lung parenchymal cells and thrombi formation. In addition SM caused congestion and hemorrhage at alveolar level. SM also caused granulovacuolar degeneration with perinuclear clumping of the cytopasm of hepatocytes and renal parenchymal cells. Renallesions were chazacterized by congestion and hemorrhage. Among visceral tissues, maximum atrophywas observed in spleen. Distribution of lesions increased with post exposure period. The maximum lesions were observed at 7th day post-exposure.
