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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 ]
The disorder may contribute to the chronic multisymptom illnesses of the Gulf War veterans [3] [4] as well as aerotoxic syndrome (especially tricresyl phosphate poisoning) The exact cause of the syndrome is unknown, although it has been associated with inhibition of patatin-like phospholipase domain-containing protein 6 (PNPLA6, aka neuropathy ...
Neurotoxicity is a form of toxicity in which a biological, chemical, or physical agent produces an adverse effect on the structure or function of the central and/or peripheral nervous system. [1] It occurs when exposure to a substance – specifically, a neurotoxin or neurotoxicant – alters the normal activity of the nervous system in such a ...
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.
Dimethoate is a widely used organophosphate insecticide and acaricide. It was patented and introduced in the 1950s by American Cyanamid. Like other organophosphates, dimethoate is an acetylcholinesterase inhibitor which disables cholinesterase, an enzyme essential for central nervous system function. It acts both by contact and through ingestion.
Furthermore, certain organophosphates can cause OPIDN, organophosphate-induced delayed polyneuropathy. This is a disease, which is characterized by degeneration of axons in the peripheral and central nervous system. This disease will show a few weeks after contamination with the organophosphate.
Chronic solvent-induced encephalopathy (CSE) is a condition induced by long-term exposure to organic solvents, often—but not always—in the workplace, that lead to a wide variety of persisting sensorimotor polyneuropathies and neurobehavioral deficits even after solvent exposure has been removed.
P–S single bonds can be generated through a variety of approaches, starting from thiols, disulfides, sulfinic acids as sulfur sources and various P(III) and P(V) coupling partners. [3] PS–C bonds can also be formed through many comparable approaches, usually by alkylating a free phosphorus-thioate anion or thioic acid.