A Review on the Radioprotective Activity of organogermanium and Organosilicon Compounds.

The present review describes the work carried out during the last 20 years in the field of the radioprotective activity and toxicity of several classes of organosilicon and organogermanium compounds (i.e. metallathiazolidines, metalladithioacetals, metallatranes and germathianes).

[The threat represented by toxins: myth or reality?].

The reasons underlying our fear of the use of toxins as new weapons different from chemical agents are discussed together with the conditions required for their use on the battlefield. The undeniable scientific contribution of toxins as pharmacological tools for the study of neurosciences and disease genesis and their prophylaxis is emphasized. In conclusion, the threat for mankind constituted by proliferation of this novel class of agents is stressed.

GK 11: promising additional neuroprotective therapy for organophosphate poisoning.

Recent experiments with primates have demonstrated that treatment with atropine/pralidoxime/diazepam, even if administered immediately after organophosphate exposure, does not totally prevent neuronal brain damage. Using primates, we have studied, for the first time, the ability of GK-11 (gacyclidine), an antiglutamatergic drug in the process of agreement for human use, given as an additional therapy, to counteract the neuropathology due to organophosphate exposure that persists after classical treatment with oxime/atropine/benzodiazepine. We have also examined the recovery of the organophosphate-intoxicated primates.

Compared toxicity of the potassium channel blockers, apamin and dendrotoxin.

The central toxicities of two potassium ion channel blockers, apamin and alpha-dendrotoxin (DTx), have been compared. Both apamin and dendrotoxin injected intracerebroventricularly produced signs of poisoning, including tremor and ataxia; however, only DTx produced changes in brain electrical activity, with high voltage spikes and epileptiform activity and subsequent brain damage. DTx, but not apamin, increased the amplitude of evoked field potentials and caused repetitive firing of neurones in hippocampal slices.

[Prevention and treatment of status epilepticus induced by soman].

Treatment of the convulsive and neuropathologic actions of organophosphates comprise the major unsolved problem in defending against this class of chemical nerve agents. Understanding and preventing these central actions are important goals of chemical defense research. It is generally accepted that inhibition of acetylcholinesterase results in an accumulation of acetylcholine (ACh) which may be responsible for the acute toxic effects of nerve agents.