Editing Soman (section)

==Metabolism==
Once taken up in the human body, soman not only inhibits AChE, but it is also a substrate for other esterases. Reaction of soman with these esterases allows for the detoxication of the compound. No metabolic toxification reactions are known for soman.

Soman can be hydrolyzed by a so-called A-esterase, more specifically a diiso{{shy}}propyl{{shy}}fluoro{{shy}}phosphatase. This esterase, also called somanase, reacts with the anhydride bond between phosphorus and fluorine and accounts for the hydrolysis of the fluoride. Somanase also hydrolyses the methyl group of soman resulting in the formation of pinacolyl methyl{{shy}}phosphonic acid (PMPA), which is a less potent AChE inhibitor.<ref name=":0">{{Cite journal|last=Jokanović|first=M.|date=2001-09-25|title=Biotransformation of organophosphorus compounds|journal=Toxicology|volume=166|issue=3|pages=139–160|issn=0300-483X|pmid=11543910|doi=10.1016/s0300-483x(01)00463-2}}</ref><ref name=":1">{{Cite journal|last=Jokanović|first=Milan|date=2009-07-10|title=Current understanding of the mechanisms involved in metabolic detoxification of warfare nerve agents|journal=Toxicology Letters|volume=188|issue=1|pages=1–10|doi=10.1016/j.toxlet.2009.03.017|issn=1879-3169|pmid=19433263}}</ref>

Soman can also bind to other [[esterase]]s, e.g., [[Acetylcholinesterase|AChE]], [[cholinesterase|cholin{{shy}}esterase]] (ChE) and [[carboxylesterase|carboxyl{{shy}}esterase]]s (CarbE). In this binding, soman loses its fluoride. After binding to AChE or ChE soman also loses its phosphoryl group, leading to the formation of [[methylphosphonic acid|methyl{{shy}}phosphonic acid]] (MPA). Binding to CarbE reduce the total concentration of soman in the blood, thus resulting in a lower toxicity. Furthermore, CarbE are involved in the detoxication by [[Hydrolysis|hydrolysing]] soman to PMPA. So CarbE account for the detoxication of soman in two ways.<ref name=":0" /><ref name=":1" />

The importance of the detoxication of soman after exposure was illustrated in experiments of Fonnum and Sterri (1981). They reported that only 5% of [[Median lethal dose|LD50]] inhibited AChE in rats, resulting in acute toxic effects. This shows that metabolic reactions accounted for the detoxification of the remaining 95% of the dose.<ref>{{cite journal | author = Fonnum, F. |author2 = Sterri, S.H. | year = 1981 | title = Factors modifying the toxicity of organophosphorus compounds including soman and sarin | journal = Fundam. Appl. Toxicol. | volume = 1 | pages = 143–147 | doi = 10.1016/S0272-0590(81)80050-4 | pmid = 7184780 | issue = 2}}</ref>

[[File:Metabolisim of Soman.png|framed|center|The metabolism of soman.]]