Abstract
Summary and conclusion
It was concluded that a major portion of intravenously injected HN2 passes through the liver of the animal. There, metabolic alterations, possibly other than simple de-alkylations, take place which lead to the biliary or lymphatic excretion of compounds the toxicity of which is greatly attenuated. It was demonstrated, however, that a single passage of the drug through the liver does not suffice to influence mortality rate due to an LD50 dose significantly. Detoxication of HN2 or its immediate metabolites in the liver, does not proceed at a sufficiently rapid rate to change the clinical course of mustard intoxication. This substantiates our previous observations which indicated that the effects of the drug on the organism are initiated quite rapidly following its administration.
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