Once taken up in the human body,<unk>  not only inhibits AChE, but it is also a substrate for other esterases. Reaction of<unk>  with these esterases allows for the detoxication of the compound. No metabolic toxification reactions are known for<unk> .<unk>  can be hydrolyzed by a so-called A-esterase, more specific a diisopropylfluorophosphatase. This esterase, also called<unk> ase, reacts with the anhydride bond between phosphorus and fluorine and accounts for the hydrolysis of the fluoride.<unk> ase also hydrolyses the methyl group of<unk>  resulting in the formation of pinacolyl methylphosphonic acid (PMPA), which is a less potent AChE inhibitor.<unk>  can also bind to other esterases, e.g., AChE, cholinesterase (ChE) and carboxylesterases (CarbE). In this binding,<unk>  loses its fluoride. After binding to AChE or ChE<unk>  also loses its phosphoryl group, leading to the formation of methylphosphonic acid (MPA). Binding to CarbE reduce the total concentration of<unk>  in the blood, thus resulting in a lower toxicity. Furthermore, CarbE are involved in the detoxication by hydrolysing<unk>  to PMPA. So CarbE account for the detoxication of<unk>  in two ways. The importance of the detoxication of<unk>  after exposure was illustrated in experiments of Fonnum and Sterri (1981). They reported that only 5% of 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. The metabolism of<unk> .
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