Abstract
1. The changes of cholinesterase activity in rabbit blood, peripheral tissues and the central nervous system following transfusion of erythrocytes with soman inhibited acetylcholinesterase we were demonstrated. 2. After incubation with soman for 0.5 or 24 h, erythrocytes without acetylcholinesterase activity were injected to intact rabbits and cholinesterase activity in the erythrocytes, plasma, diaphragm, liver and various parts of the brain were evaluated 24 h following blood-transfusion. 3. When erythrocytes were incubated with soman for 24 h, no changes of cholinesterase activity in the rabbit following blood-transfusion were observed with an exception of erythrocyte acetylcholinesterase. 4. When erythrocytes were incubated with soman for 0.5 h, a significant decrease in cholinesterase activity in the erythrocytes, plasma, diaphragm and liver following blood-transfusion was found. These data show that soman is able to release from erythrocytes and inhibit cholinesterase activities not only in vitro but also in vivo although the significant inhibition of cholinesterase activities by soman was only observed in the peripheral compartment.
Highlights
In spite of a good knowledge of the basic mechanism of nerve agent toxic effects, the treatment of acute intoxication with nerve agents has not been satisfactorily efficacious yet (3)
After incubation with soman for 0.5 or 24h, erythrocytes without acetylcholinesterase activity were injected to intact rabbits and cholinesterase activity in the erythrocytes, plasma, diaphragm, liver and various parts of the brain were evaluated 24h following blood-transfusion
When erythrocytes were incubated with soman for 24h, no changes of cholinesterase activity in the rabbit following blood-transfusion were observed with an exception of erythrocyte acetylcholinesterase
Summary
In spite of a good knowledge of the basic mechanism of nerve agent toxic effects, the treatment of acute intoxication with nerve agents has not been satisfactorily efficacious yet (3). Soman (pinacolyl methylphosphonofluoridate) is really resistant to antidotal treatment (7,8,10). Soman differs from many other organophosphates in the rate of aging and in the existence of a depot in the organism (2). The rapid process of aging, that means the monodealkylation of soman-inhibited acetylcholinesterase (AChE, EC 3.1.1.7), prevents both the spontaneous reactivation and the reactivation induced by oximes (2,5). The existence of a soman depot in the organism can influence soman poisoning because soman can be released from the depot and cause a new attack of intoxication. This depot was described for the skin, muscles and lung (2,6)
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
