These liquids are tasteless, odorless and volatile, and evaporate spontaneously at room temperature. The G agents have the density of water and evaporate at about the same rate as dose water, and have freezing points around 0°C and boiling points around 150°C. The VX, in contrast, are oily, have a consistency similar to that of motor oil, and evaporate very slowly. Thus, it will contaminate the environment for Inhibitors,research,lifescience,medical a longer period.13 Toxicokinetics Organophosphorous compounds can easily cross the respiratory epithelial and dermal membranes because of their lipophilic structures, and thus they are formed mostly
as aerosol.14,15 Gastric mucosa is also very permeable to Ops, Inhibitors,research,lifescience,medical and is a classical way of absorption in suicidal cases.16 Organophosphorous compounds
are distributed in the whole body, particularly in fatty tissues, and their fast degradation usually inhibits their accumulation. Some OPs are selleck inhibitor eliminated without considerable metabolism. However, they usually become degraded and eliminated in urine, feces and exhaled air. Most OP Inhibitors,research,lifescience,medical insecticides are activated through oxidation in the liver by enzymes of cytochrome P450 system and flavin-containing monooxygenases. Soman, sarin and other nerve agents are inherently active. The main enzymatic systems involved in the detoxification of OPs are phosphotriesterases, carboxylesterases and glutathione-S-transferases. A main detoxification pathway of Inhibitors,research,lifescience,medical OPs is hydrolysis by esterases
called ‘phosphotriesterases’ (PTEs). The products of the reaction display no phosphorylating capability, and therefore the hydrolysis of OPs by PTEs is considered a detoxification. The most known PTEs is human serum paraoxonases.17 Compared to G-agents, VX has several particular characteristics. The anticholinesterase properties of VX are as a result of the oxo Inhibitors,research,lifescience,medical (O) group, and partly the presence of alkyl substituents. The VX is present in blood as a protonated amine. It is hydrolyzed at a slower rate than G-agents, and reacts more slowly with CarbE and A-esterases. The VX is also metabolized by other pathways like oxidation reactions first at nitrogen and/or sulfur.18 Shih et al. studied the excretion pattern of alkyl methylphosphonic acids from sarin, soman and cyclosarin in the rat following subcutaneous administration with a dose of 0.075 mg/kg.19 Urinary excretion over the first 24 h constituted nearly 90% of the sarin and cyclosarin. Soman was eliminated with a slower and biphasic elimination curve. Approximately 50% was excreted within the first 24 h. The initial hydrolysis of tabun produces ethyl N, N-dimethylphosphoramidic acid and ethyl phosphorocyanidic acid, that are unstable and hydrolyze further to ethyl phosphoric acid and then slowly to phosphate. But the problem is that the background of ethyl phosphoric acid in the general population is quite variable, presumably from pesticides and plasticizers.