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Organophosphate poisoning is poisoning due to organophosphates (OPs). [4] Organophosphates are used as insecticides , medications, and nerve agents . [ 4 ] Symptoms include increased saliva and tear production, diarrhea , vomiting, small pupils , sweating, muscle tremors, and confusion. [ 2 ]
In the treatment of organophosphate toxicity, cholinesterase reactivators such as Pralidoxime reactivate inhibited AChE at peripheral nicotinic receptors.Since AChE mediates effects on both nicotinic and muscarinic receptors, cholinesterase reactivators are co-administered with muscarinic antagonists, primarily atropine.
Pralidoxime (2-pyridine aldoxime methyl chloride) or 2-PAM, usually as the chloride or iodide salts, belongs to a family of compounds called oximes that bind to organophosphate-inactivated acetylcholinesterase. [1] It is used to treat organophosphate poisoning [2] in conjunction with atropine and either diazepam or midazolam. It is a white solid.
Organophosphate poisoning is not common in the developed world. Most cases of terbufos poisoning occur in the developing world, where protection against pesticides is scarce, but compounds such as terbufos are widespread, uncontrolled by a government and readily available for farmers.
Obidoxime is a member of the oxime family used to treat organophosphate poisoning. Oximes are drugs known for their ability to reverse the binding of organophosphorus compounds to the enzyme acetylcholinesterase (AChE). [1] AChE is an enzyme that removes acetylcholine from the synapse after it creates the required stimulation on the next nerve ...
Asoxime chloride, or more commonly HI-6, is a Hagedorn oxime used in the treatment of organophosphate poisoning. [1] See also. Obidoxime; Pralidoxime; References
This results in abnormal accumulation of ACh within the nervous system. Diazinon, although a thiophosphoric ester, shares a common mechanism of toxicity with other organophosphate insecticides such as chlorpyrifos, malathion and parathion, and is not very effective against the organophosphate-resistant insect populations. [citation needed]
The toxicity of chlorfenvinphos is primarily caused by its inhibition of cholinesterase activity. Chlorfenvinphos reacts with the acetylcholine binding sites of enzymes that hydrolyze acetylcholine, thereby preventing their catalysis of this reaction. The reaction itself is a phosphorylation, which is reversible. The phosphorylated enzymes can ...