Neuro-endocrine toxicity

Shulga V., Delayed neuro-endocrine toxicity indused by organophosphorus compounds-natural consequence of poisonous substances application for terrorist purpose , In Medical Aspects of Chemical and Biological Terrorism -Chemical Terrorism and Tramautism, Alexander Monov and Christophor Dishovsky, eds, Publishing House of the Union of Scientists in Bulgaria, 2005 ( in press). 

Delayed Neuro-Endocrine Toxicity induced by Organophosphorus Compounds - Natural Consequence of Poisonous substances Application for Terrorist Purposes... 

Shulga discusses in his paper the possibility for development of the typical delayed syndrome of the neuro-endocrine toxicity after intoxication with OPC. 

This is another evidence to conclude that delayed consequences are in direct relation to the damages inflicted on the central nervous system subcortical structures. No doubt, a definite limit of affection of subcortical structures exists, beyond which the course of intoxication will be confused. Under limit of affection one should understand not so much the intensity, but the time period during which the poisonous substances were applied intra-venal application, as compared to prolonged, for example skin resorption, has decreased effect in the formation of delayed neuro-endocrine toxicity. 

The involvement of the medula oblongata and the other subcortical structures, the centre of hypotalanuc integration as well - as a result of the anticholinesterase (possible and direct) effect of the poisonous substance on them - can be considered as the triggering mechanism for the development of severe consequences of non anticholinesterase nature, having in a number of cases a lethal outcome. In this case - pathogenesis of delayed neuro-endocrine toxicity. 

The delayed neuro-endocrine toxicity was observed at the rate of one of five persons affected by the OPC in the Gulf War , as in the Japanese tragedies. Analogical rate was observed in the model of the animal s experiments. 

The clinical course of the delayed neuro-endocrine toxicity and the typical manifestations with prevalence of neuro-endocrine pathology appears very similar in animal experiments and in real conditions in men. 

It should be underlined that in Matsumoto the number of victims on the account of the delayed neuro-endocrine toxicity grew from 200 to 600 people, i.e. three times, while in the conditions of the Tokyo metro - from 5000 to 6000, i.e. 20%. 

For the remaining people, about 7000, there is no doubt that, beside the panic and the stress conditions, the excessively small concentrations also played their role and had their share, but did not induce development of the typical delayed syndrome of the neuro-endocrine toxicity. 

Consequently, the reason for developing delayed neuro-endocrine toxicity is not exposure to extremely small doses , but to doses, exceeding considerably the safe concentration levels. 

In this respect, treatment with cholinolytic antidote drugs and cholinesterase reactivators does not block the rise, course and outcome of the delayed neuro-endocrine OPC toxicity. 

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