Histobiochemical changes in lung of protein deficient rats following repeated exposures of MIC vapour.

Adult male albino rats, maintained on normal or protein deficient diets from weanling, were exposed to repeated doses of MIC vapour (0.32 mg/L for 8 min for 5 consecutive days) under static conditions. Histopathology and the activities of alkaline and acid phosphatases and GSH content of lung were studied upto day 14 after exposure. Mild but repeated exposures of MIC vapour caused severe pulmonary lesions like denudation of bronchiolar epithelial lining tissue, cellular infiltration, edema, emphysema followed by hyperplasia, hypertrophy, fibrosis and intraluminal fibroplasia. The activities of alkaline and acid phosphatases were increased at earlier intervals while GSH content decreased significantly and remained low throughout the experimental duration. Protein deficiency was found to aggravate the toxic potentials of MIC in present condition.

Acute histopathological changes induced by methyl isocyanate in lungs, liver, kidneys & spleen of rats.

Methyl isocyanate (MIC), inhaled or administered subcutaneously (sc) at lethal concentration/dose caused essentially similar histopathological changes in all the viscera except for the lungs. The observed congestion of the viscera, foci of hepatocellular necrosis with widening of Disse's spaces in the liver and tubulo-rhexis with degeneration in the kidneys are attributable mostly to the initial shock. In addition, the lungs revealed more distinct route specific patterns of histopathological lesions. Inhaled MIC caused acute eosinophilic necrosis of the bronchial epithelium and frank alveolar edema, while MIC administered sc led to prominent vascular endothelial damage and severe interstitial pneumonitis with normal bronchial epithelium. The differential loci of damage in the lungs may be attributed to the immediate contact surface available for interaction with MIC.