3-Nitropropionic acid and similar nitrotoxins.

3-Nitropropionic acid as well as 3-nitro-1-propanol and its beta-D-glucopyranoside (miserotoxin) are the plant and fungal toxins reported to interrupt mitochondrial electron transport resulting in cellular energy deficit. These nitrotoxins induce neurological degeneration in ruminants and humans. 3-Nitropropionic acid-intoxicated rats serve as the animal model for Huntington's disease.

A comparison of the efficacy of new monopyridinium oximes with the oxime HI-6 against mevinphos in mice.

1. The therapeutic efficacy of three new monopyridinium oximes (2,4-PAEtM, 2,5-PAEtM, 2,5-PAAM) and the bispyridinium oxime HI-6 was evaluated in combination with benactyzine against acute poisoning with the organophosphorus insecticide mevinphos in mice. 2. When mice were treated two min after mevinphos poisoning, no significant differences in the therapeutic effectiveness of tested oximes were observed. They increased the 24h LD50 values of mevinphos about three times in comparison with non-treated intoxicated animals. 3. On the other hand, there were significant differences in their therapeutic efficacy when they were administered 30 sec following mevinphos challenge. The monopyridinium oxime 2,5-PAEtM seems to be the most efficacious against mevinphos toxicity. 4. Use of new monopyridinium oxime 2,5-PAEtM appears to be the improvement in the antidotal treatment of poisoning with organophosphorus insecticide mevinphos in comparison with HI-6.

The efficacy of monopyridinium (2-PAAM, 2-PAEM) and bispyridinium (obidoxime, HI-6) oximes against mevinphos in mice.

The efficacy of two new monopyridinium oximes (2-PAAM, 2-PAEM) and two bispyridinium oximes (obidoxime. HI-6) was tested in combination with atropine sulphate against acute poisoning with the organophosphorus insecticide mevinphos in mice. When mice were treated two min. after mevinphos poisoning, no significant differences in the therapeutic effect of tested oximes were observed. The oximes increased the 24 hr LD50 values of mevinphos about two times in comparison with the 24 hr LD50 values of mevinphos in mice protected with atropine sulphate alone and more than three times in comparison with non-treated intoxicated animals. On the other hand, both monopyridinium oximes were significantly more efficacious than HI-6 and as efficacious as obidoxime when they were administered 30 sec. after mevinphos poisoning. Both monopyridinium oximes and obidoxime increased the 24 hr values of mevinphos almost three times in comparison with the 24 hr values of mevinphos in mice protected with atropine sulphate alone and about twenty-five times in comparison with non-treated intoxicated animals, while the oxime HI-6 less than two times in comparison with the 24 hr values of mevinphos in mice protected with atropine sulphate alone and about fifteen times in comparison with non-treated intoxicated animals. Use of new monopyridinium oximes seems to be the improvement in the antidotal treatment of poisoning with organophosphorous insecticide mevinphos in comparison with HI-6 but not in comparison with obidoxime when oximes are used in equimolar doses.

[Biotransformation of the anticholinesterase agent, 9-amino-7-methoxy-1,2,3,4-tetrahydroacridine]. / Biotransformacní studie anticholinesterazika 9-amino-7-methoxy-1,2,3,4-tetrahydroakridinu.

Biotransformation of the anticholinesterasic agent 9-amino-7-methoxy-1,2,3,4-tetrahydroacridine was studied in the laboratory rat. In the animal urine, the main identified metabolites were 9-amino-7-hydroxy-1,2,3,4-tetrahydroacridine and its conjugate with glucuronic acid, or sulfuric acid, as well as 9-amino-1-hydroxy-7-methoxy-1,2,3,4-tetrahydroacridine and 9-amino-2-hydroxy-7-methoxy-1,2,3,4-tetrahydroacridine. A part of the drug was excreted in an unchanged form.

Role of interaction of the tanycytes of the third ventricle of the brain with the vascular bed endothelium in enzymatic activation of the parkinsonism-inducing proneurotoxin MPTP in rat brain.

The authors describe the localization of monoaminooxidases oxidizing the protoxin MPTP to the active neurotoxic MPP+ ion, which induces parkinsonism by destroying the dopaminergic neurons of the nigrostriatum. Apart from some types of magnocellular neurons of the hypothalamus, enzymatic activity is localized in the endothelium of segments of the circumventricular vascular bed communicating with the enzymatically equally positive processes of the tanycytes of the third brain ventricle. The findings are briefly discussed from the aspect of the pathogenesis of experimental parkinsonism.