Biological monitoring of exposure to nerve agents
Language English Country England, Great Britain Media print
Document type Journal Article
PubMed
1390271
PubMed Central
PMC1039310
DOI
10.1136/oem.49.9.648
Knihovny.cz E-resources
- MeSH
- Acetylcholinesterase blood MeSH
- Diaphragm enzymology MeSH
- Rats MeSH
- Brain enzymology MeSH
- Organophosphorus Compounds toxicity MeSH
- Organothiophosphorus Compounds toxicity MeSH
- Dogs MeSH
- Salivation MeSH
- Sarin toxicity MeSH
- Soman toxicity MeSH
- Seizures chemically induced MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Dogs MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Names of Substances
- 2-dimethylaminoethyl(dimethylamido)phosphonofluoridate MeSH Browser
- Acetylcholinesterase MeSH
- Organophosphorus Compounds MeSH
- Organothiophosphorus Compounds MeSH
- Sarin MeSH
- Soman MeSH
- VX MeSH Browser
Changes in acetylcholinesterase activity in blood and some organs of rats after intoxication with sarin, soman, VX, and 2-dimethylaminoethyl-(dimethylamido)-phosphonofluoridate (GV), in doses of roughly 2 x LD50 given intramuscularly, were obtained from published data and by experiment. The time course of inhibition of acetylcholinesterase in blood, regions of brain, and diaphragm and the occurrence of signs and symptoms of poisoning (none, salivation, disturbed ventilation and fasciculations, convulsions, or death) were summarised and compared. When blood enzyme activities were 70-100% normal, no obvious signs were seen; at 60-70%, salivation occurred; at less than 30-55%, disturbed ventilation and fasciculations were seen, and at 15-30%, convulsions occurred. Less than 10% was fatal. In experiments with narcotised dogs, the blood acetylcholinesterase activity and the ability to reactivate it with trimedoxime were determined after intoxication by intramuscular administration of the four compounds. It is concluded that acetylcholinesterase activity in the blood corresponds to that in the target organs and can be considered as an appropriate parameter for biological monitoring of exposure to nerve gases. Moreover, determination of reactivation of blood acetylcholinesterase gives more information than simple determination of enzyme activity.
See more in PubMed
Arch Toxicol. 1989;63(2):150-4 PubMed
Drug Chem Toxicol. 1988;11(3):289-305 PubMed
Proc Soc Exp Biol Med. 1973 Nov;144(2):725-30 PubMed
Br Med Bull. 1969 Sep;25(3):236-40 PubMed
Biochem Pharmacol. 1961 Jul;7:88-95 PubMed
Toxicology. 1989 Aug;57(3):241-54 PubMed
Pharmacol Toxicol. 1989 Sep;65(3):181-4 PubMed
Toxicol Lett. 1988 Oct;43(1-3):175-88 PubMed
Toxicol Appl Pharmacol. 1987 Mar 30;88(1):66-76 PubMed
Biochem Pharmacol. 1972 Mar 1;21(5):687-94 PubMed
Br J Pharmacol. 1972 Jun;45(2):368-71 PubMed
Biochem Pharmacol. 1965 May;14(5):641-50 PubMed