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Organophosphorous compounds have been employed as pesticides and chemical warfare nerve agents. Toxicity of organophosphorous compounds is a result of excessive cholinergic stimulation through inhibition of acetyl cholinesterase. Clinical manifestations include cholinergic syndromes, central nervous system and cardiovascular disorders. Organophosphorous pesticide poisonings are common in developing worlds including Iran and Sri Lanka.
Nerve agents were used during the Iraq-Iran war in and in a terrorist attack in Japan in Following decontamination, depending on the severity of intoxication the administration of atropine to counteract muscarinic over-stimulation, and an oxime to reactivate acetyl cholinesterase are indicated. Supportive and intensive care therapy including diazepam to control convulsions and mechanical respiration may be required.
Recent investigations have revealed that intravenous infusion of sodium bicarbonate to produce mild to moderate alkalinization is effective. Gacyclidine; an antiglutamatergic compound, was also proved to be beneficial in conjunction with atropine, pralidoxime, and diazepam in nerve agent poisoning.
Intravenous magnesium sulfate decreased hospitalization duration and improved outcomes in patients with organophosphorous poisoning. Bio-scavengers including fresh frozen plasma or albumin have recently been suggested as a useful therapy through clearing of free organophosphates. Hemofiltration and antioxidants are also suggested for organophosphorous poisoning. Recombinant bacterial phosphotriesterases and hydrolases that are able to transfer organophosphorous-degrading enzymes are very promising in delayed treatment of organophosphorous poisoning.
Recently, encapsulation of drugs or enzymes in nanocarriers has also been proposed. Given the signs and symptoms of organophosphorous poisoning, health professionals should remain updated about the recent advances in treatment of organophosphorous poisoning poisonings. Organophosphorous OPs compounds have been employed as pesticides, petroleum additives and chemical warfare nerve agents. It is believed that between , and 3,, OP poisoning occur globally every year.
Mortality is higher in the developing countries where OP pesticides are readily available and may be used for suicide. They are estimated to cause , fatalities annually. For the first time, OPs were synthesized by von Hoffman.
In He synthesized methyl phosphor chloride, which led to the synthesis of a number of insecticides. The nerve agents comprise two series including G-agents and V-agents. G-agents were produced in Germany by Dr.
Gerhard Schrader team in s. They synthesized tabun in and then sarin. The G agents comprise fluorine compounds of organophosphate except for tabun GA.
The famous agents in this group are sarin GB; 2-fluoro-methylphophoryloxypropane , soman GD; 3-fluoro-methyl-phosphoryloxy-2, 2-dimethyl-butane , tabun GA; ethyl N, N-dimethylphophoramidocyanidate and cyclosarin GF; fluoro-methyl-phophoryloxycyclohexane. The V agents are sulfur containing organophosphate compounds. The V-agents are more toxic than the G-agents.
Nerve agent tabun was used in the battlefield for the first time in by Iraqi army to achieve victory against Iran. From to , Iraq used sulfur mustard and nerve agents such as sarin and tabun against Iranian combatants, and later against the civilians.
Nerve agents were also used by Iraq in against Iraqi Kurdish civilians during Halabjah massacre. It was estimated that 45, to , individuals were poisoned by chemical weapons during the Iraq-Iran war. The poisoning, which was associated with high mortalities, was mostly caused by the nerve agents.
Despite the establishment of organization for prohibition of chemical weapons OPCW , OP nerve agents are still threat to the human population. In addition, wide use of OP pesticides in most developing countries including Iran has induced health problems.
Hence, it is quite logical that health professionals should increase their knowledge about all aspects of OPs, particularly on recent advances in the treatment of pesticides and nerve agent poisonings. Organophosphorous compounds including organophosphates are chemically derived from phosphoric, phosphonic, phosphinic or thiophosphoric acids.
Organophosphates are usually esters, amides, or thiol derivatives of phosphoric, phosphonic, or phosphinic acids. The general formula of organophosphates is as follows:. Organophosphorous pesticides vary in chemical structures and toxicities.
The main groups are phosphate, phosphorothioate, O-alkyl phosphorothioate and phosphorodithioate. A phosphorthioate compound such as parathion is much more toxic than a phosphorodithioate compound like Malathion.
Apart from the OP pesticides and chemical warfare nerve agents, very few OP compounds such as glyphosate and merphos were used as herbicides. Organophosphorous herbicides differ from the OP pesticides structurally and their AChE—inhibiting power is much less than the other OPs.
This misunderstanding comes from the first use in World War I of CWA such as chlorine and phosgene that are true gases. These liquids are tasteless, odorless and volatile, and evaporate spontaneously at room temperature. 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 a longer period. Organophosphorous compounds can easily cross the respiratory epithelial and dermal membranes because of their lipophilic structures, and thus they are formed mostly as aerosol.
Some OPs are eliminated without considerable metabolism. However, they usually become degraded and eliminated in urine, feces and exhaled air. Most OP insecticides are activated through oxidation in the liver by enzymes of cytochrome P 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.
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. Compared to G-agents, VX has several particular characteristics.
The anticholinesterase properties of VX are as a result of the oxo 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.
Soman was eliminated with a slower and biphasic elimination curve. 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. The Remnant of unbound OP in patients depends on the chemical properties and activity of OP hydrolyzing enzymes, like paraoxonases.
Lipophilic OP compounds such as parathion and its active form paraoxon, may distribute widely in the body resulting in long-term toxic plasma levels. Toxicity of OPs is the result of excessive cholinergic stimulation through inhibition of acetyl cholinesterase AChE.
Muscarinic and nicotinic acetylcholine ACh receptors are found in the central and peripheral nervous system. Acetylcholine is a neurotransmitter that contributes to nerve conduction following its release in autonomic ganglia at sympathetic preganglionic synapses, at parasympathetic postganglionic synapses, and at neuromuscular junctions of the skeletal muscle.
In human body there are different types of cholinesterases, which differ in their location in tissues, substrate affinity, and physiological function. Two main types of cholinesterases include: Acetyl cholinesterase is the principal form that is found in neurons, neuromuscular junctions and erythrocyte membranes. Another form of AChE, which is known as serum cholinesterase ChE , is a group of enzymes present in plasma, liver, cerebrospinal fluid and glial cells.
It is a circulating plasma glycoprotein synthesized in the liver, and does not serve any known physiological function. Butyrylcholinesterase acts as a stoichiometric scavenger of nerve agents and its inhibition appears to have no significant physiological effects in the absence of other toxicants.
It is also important as a biomarker of exposure to OPs. Nerve agents react rapidly with a serine hydroxyl group in the active site of AChE and form a phosphate or phosphonate ester.
The G-agents are anticholinesterase OP nerve agents that at sufficient concentrations can be toxic or fatal by any route of exposure. Phosphorylated AChE is not able to hydrolyze ACh, and regenerates very slowly, thus, the enzyme will remain inhibited until new enzyme is generated, or until an enzyme reactivator oxime is used.
It has also been reported that at very high doses of nerve gases, they can activate AChE receptors. After binding to AChE and BChE the phosphoryl residues of soman, sarin, tabun and VX undergo an intramolecular rearrangement with subsequent loss of one phosphoryl group.
This reaction is known as aging The time between OP exposure and the irreversible phosphorylation , and defined as non-enzymatic time-dependent loss of one alkyl group bound to the phosphorus, which leads to a stable non-receivable form of phosphorylated AChE that is resistant to both spontaneous and oxime-induced reactivation. The aging varies from a few minutes soman to 22 hours cyclosarin. As inhibitors of AChE, Organophosphorous compounds, may act directly or indirectly. Direct inhibitors, such as dichlorvos, are useful without additional metabolic modification following absorption, and thus cause rapid symptoms and signs during or after exposure.
To be effective, indirect inhibitors such as malathion need to be transformed. The symptoms and signs of these compounds appear later, and last longer. In addition, due to the reversibility of the binding reaction of sarin and soman to CarbE, it appears that CarbE is involved in metabolic detoxification of these agents to their corresponding non-toxic metabolites isopropyl methylphosphonic acid IMPA and pinacolyl methylphosphonic acid PMPA.
Organophosphorous compounds poisoning can be diagnosed based on a history of exposure via intentional or accidental oral OP pesticide ingestion, occupational or chemical warfare assult, and clinical manifestations.
The enzymes inhibited by OPs provide specific biomarkers of exposure, until the turnover of the enzyme in favorable cases. Screening the red blood cell concentrations of AChE in individuals who are exposed to these agents is essential. Although screening has several limitations, it can also be used for suspected individuals with nerve agent poisoning.
Due to interindividual variations, it does not provide a reliable evidence for low levels of organophosphate exposure at low levels due to interindividual variations. Moreover, control activity levels are often not available. However, measurement of AChE inhibition is still the most widely used method for the assessment of exposure to nerve agents. Severity grading of organophosphorus poisoning based on the cholinesterase inhibition and atropine dose required for atropinization. Urine metabolites, or adducts to proteins and DNA can also be used as biomarkers for detecting nerve agent exposure.
The main metabolites of nerve agents are alkyl methylphosphonic acids that are found rapidly in the urine, and can be detected up to one week after exposure depending on the extent of eposure.
A biosensor which is a potentiometer enzyme electrode has been developed to determine OP nerve agents directly.
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Recent Advances in the Treatment of Organophosphorous Poisonings
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