ABSTRACT
The aim of this study was to demonstrate changes in acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE) activities, tyrosine aminotransferase activity (TAT) and plasma corticosterone level, neuroexcitability and behavior following 24 hours and 4 weeks of soman sublethal inhalation exposure at low level. AChE activity in erythrocytes and BuChE activity in plasma was decreased (dependent on the concentration of soman) 24 h and 4 weeks after the exposure. Similar decrease in AChE activity in different brain parts was observed. One of stressogenic parameters (TAT) was changed after 24 h exposure only. 4 weeks after the exposure, these parameters (corticosterone and TAT) were in the range of normal values. Behaviour of experimental animals was changed 24 h after the exposure persisting 4 weeks after the exposure as well as neuroexcitability.
Subject(s)
Acetylcholinesterase/metabolism , Behavior, Animal/drug effects , Butyrylcholinesterase/metabolism , Chemical Warfare Agents/toxicity , Cholinesterase Inhibitors/toxicity , Cholinesterases/metabolism , Soman/toxicity , Tyrosine Transaminase/metabolism , Acetylcholinesterase/blood , Animals , Brain/enzymology , Butyrylcholinesterase/blood , Cholinesterases/blood , Corticosterone/blood , Diaphragm/enzymology , Erythrocytes/enzymology , Female , Guinea Pigs , Inhalation Exposure , Lethal Dose 50 , Liver/enzymology , Tyrosine Transaminase/bloodABSTRACT
Pharmacological pretreatment and antidotal treatment on tabun-induced neurotoxicity were studied in male albino rats that were poisoned with a lethal dose of tabun (280 microg/kg i.m.; 100% of LD50 value) and observed at 24 hours and 7 days following tabun challenge. The neurotoxicity of tabun was evaluated using a Functional observational battery and an automatic measurement of motor activity. Pharmacological pretreatment as well as antidotal treatment were able to reverse most of tabun-induced neurotoxic signs observed at 24 hours following tabun poisoning. However, there was not significant difference between the efficacy of profylaxis and antidotal treatment to eliminate tabun-induced neurotoxicity. The combination of profylactic pretreatment and antidotal treatment seems to be slightly more effective in the elimination of tabun-induced neurotoxicity in rats at 24 hours following tabun challenge in comparison with the administration of profylactic pretreatment or antidotal treatment alone. At 7 days following tabun poisoning, very few neurotoxic signs in tabun-poisoned rats were observed regardless of administration of pharmacological pretreatment or antidotal treatment. Thus, our findings confirm that the combination of pharmacological pretreatment and antidotal treatment is not only able to protect the experimental animals from the lethal effects of tabun but also to eliminate most of tabun-induced signs of neurotoxicity in tabun-poisoned rats.
Subject(s)
Benactyzine/therapeutic use , Cholinesterase Inhibitors/toxicity , Neuroprotective Agents/therapeutic use , Organophosphates/toxicity , Pyridostigmine Bromide/therapeutic use , Trihexyphenidyl/therapeutic use , Animals , Antidotes/therapeutic use , Behavior, Animal/drug effects , Cholinesterase Reactivators/therapeutic use , Drug Combinations , Drug Therapy, Combination , Lethal Dose 50 , Male , Rats , Rats, WistarABSTRACT
To study the influence of pharmacological pretreatment (PANPAL) and antidotal treatment (obidoxime plus atropine) on tabun-induced neurotoxicity, male albino rats were poisoned with a lethal dose of tabun (280 microg/kg i.m.; 100% of LD(50) value) and observed at 24 h and 7 days following tabun challenge. The neurotoxicity of tabun was evaluated using a functional observational battery (FOB) and an automatic measurement of motor activity. Pharmacological pretreatment as well as antidotal treatment were able to eliminate most of tabun-induced neurotoxic effects observed at 24 h following tabun poisoning. However, there was not significant difference between the efficacy of PANPAL and antidotal treatment to eliminate tabun-induced neurotoxicity in rats. The combination of PANPAL pretreatment and antidotal treatment seems to be slightly more effective in the elimination of tabun-induced neurotoxicity in rats at 24 h following tabun challenge in comparison with the administration of PANPAL pretreatment or antidotal treatment alone. At 7 days following tabun poisoning, very few neurotoxic signs in tabun-poisoned rats were observed regardless of administration of pharmacological pretreatment or antidotal treatment. Thus, our findings confirm that the combination of pharmacological pretreatment and antidotal treatment is not only able to protect the experimental animals from the lethal effects of tabun but also to eliminate most of tabun-induced signs of neurotoxicity in tabun-poisoned rats.
