Abstract
The action of HI-6 (1-[[[(4-aminocarbonyl)pyridiniol]methoxy]methyl]-2-[(hydroxyimino)methyl]pyridinium dichloride monohydrate) and obidoxime on soman-induced anticholinesterase and stressogenic effects was studied in rats. HI-6 significantly affected acetylcholinesterase inhibition in erythrocytes, brain and diaphragm and practically eliminated the stressogenic effects of soman, i.e. an increase in plasma corticosterone level and liver tyrosine aminotransferase activity, while obidoxime, on the other hand, had very little influence on soman-induced inhibition of acetylcholinesterase activity and the stressogenic effects of soman. These findings support a hypothesis that the effects of HI-6 are not solely due to reactivation of the enzyme. They also demonstrate its importance in the treatment of soman poisoning in rats.
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