Phosphoric paraoxon

Insecticides of the phosphoric acid triester class include paraoxon (9.49) and dichlorvos (9.50). The phosphorothioate derivative parathion is a relatively non-toxic insecticide that undergoes monooxygenase-catalyzed oxidative desulfuration to paraoxon [105] (see also Chapt. 7 in [59] see Sect. 9.3.6). Paraoxon itself, like its congeners and the P-halide nerve gases, is highly toxic through its potent inactivation of acetylcholinesterase [69]. 

The inactivation and detoxification of paraoxon and congeners are catalyzed by the so-called A-esterases, which, as discussed, comprise aryleste-rase (sometimes still called paraoxonase, EC 3.1.1.2) and phosphoric triester hydrolases (phosphotriesterases, EC 3.1.8) subdivided into aryldialkylphos-phatase (organophosphate hydrolase, paraoxonase, EC 3.1.8.1) and organophosphorus acid anhydrolases (EC 3.1.8.2 see Sect. 9.3.7) [65][69][106-108], These activities, which occur mostly in the mammalian liver and... 

Reported ozonation products of parathion in drinking water include sulfuric acid (Richard and Brener, 1984), paraoxon, 2,4-dinitrophenol, picric, and phosphoric acids (Laplanche et al, 1984). 

Disposition in the Body. Parathion is activated in the liver by metabolism to paraoxon. Parathion and paraoxon are further metabolised to diethylthiophosphoric acid (DETP), diethyl-phosphoric acid (DEP), and 4-nitrophenol which are the major urinary excretion products although DETP and DEP are unstable in stored urine. Urinary 4-nitrophenol concentrations may be indicative of the extent of exposure to parathion. 4-Nitrophenol is rapidly excreted in the urine and is not detectable 48 hours after exposure by inhalation or ingestion, but excretion is more prolonged after exposure of intact skin due to the much slower absorption of parathion by this route. Aminoparathion has been detected in postmortem blood and tissues. 

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