Cholinesterase inhibitors toxicity

Caution A potent cholinesterase inhibitor. Toxic effects similar to, but more intense than, parathion, q.v. See also Sarin and Tabun. 

Caution. Potent cholinesterase inhibitor. Toxic not only by inhalation bur by absorption through skin and eyes. In -halation produces constriction of pupils of the eye, difficulty in breathing followed by bronchia] constriction, convnlsions. death. 

Respiratory failure, from neuromuscular paralysis or CNS depression, is the most important cause of acute deaths in cholinesterase inhibitor toxicity. The answer is (E). 

Lockridge. O.. EKiyscn, E. G,. Voclker, T, Thomp.son, C. M., and Schopfer, L. M, 2005. Life without acetylcholinesterase The implications of cholinesterase inhibitor toxicity in AChE-knockout mice. Envirva. Toxical. Ptuirmacai. 19,463—469. 

A highly toxic substance by ingestion, and possibly by most other routes of exposure moderately toxic by inhalation and skin contact cholinesterase inhibitor toxic effects are similar to those of other carbamate pesticides and include excessive salivation, lacrimation, slow heart rate, blurred vision, twitching of muscle and lack of coordination, nausea, weakness, diarrhea and abdominal pain oral intake of probably 1.5-3 g could be fatal to adult humans a teratogenic substance, producing adverse reproductive effects in experimental animals. 

Moderately toxic by ingestion and possibly other routes of exposure cholinesterase inhibitor toxic symptoms include headache. 

An extremely toxic organophosphorus pesticide cholinesterase inhibitor. Toxic effects are similar to those of monocrotophos. Toxic symptoms include headache, dizziness, muscle spasms, blurred vision, dilation of pupil. 

Extremely toxic phosphate ester however, snsceptible to hydrolyze in acid or alkali cholinesterase inhibitor toxic properties are similar to those of dicrotophos, symptoms inclnde headache, dizziness, pinpoint pnpils, blnrred vision, weakness, mnscle spasms, vomiting, diarrhea, abdominal cramp, shortness of breath, and hypotension high expo-snre may canse seizure, coma, and respiratory paralysis. 

Highly toxic by all routes of exposure cholinesterase inhibitor toxic symptoms similar to those of Demeton and range form headache, dizziness, blurred vision, and muscle spasms to gastrointestinal effects manifesting vomiting, diarrhea, and abdominal pain, as well as respiratory symptoms of dyspnea, respiratory depression, and paralysis high exposures may result in onset of seizures and loss of consciousness absorbed readily through skin. 

Cholinesterase inhibitor toxic properties similar to those of parathion however. 

When Hie cholinesterase inhibitors are administered with the anticholinergic drugp, there is a potential decrease in activity of the anticholinergic drug. There is an increased risk of toxicity of theophylline when the cholinesterase inhibitors are administered with tacrine There is a synergistic effect when tacrine is administered with succinyl-choline, cholinesterase inhibitors, or cholinergic agonists (eg, bethanechol). 

Brief notes are added on phosphorofluoridates even though their destruction by microbial activity— though clearly possible—is limited by their toxicity to the requisite microorganisms. One of the motivations for their inclusion is the fact that the hydrolytic enzyme(s) responsible for defluorination—organophosphorus acid anhydrase (OPA)—is widespread, and is found in a number of bacteria (Landis and DeFrank 1990). The microbial hydrolysis of organophosphorus pesticides and cholinesterase inhibitors is accomplished by several distinct enzymes, which are collectively termed organophosphorus acid anhydrases (OPAs). These have been reviewed (DeFrank 1991), so that only a few additional comments are necessary. 

Oxime carbamates are generally applied either directly to the tilled soil or sprayed on crops. One of the advantages of oxime carbamates is their short persistence on plants. They are readily degraded into their metabolites shortly after application. However, some of these metabolites have insecticidal properties even more potent than those of the parent compound. For example, the oxidative product of aldicarb is aldicarb sulfoxide, which is observed to be 10-20 times more active as a cholinesterase inhibitor than aldicarb. Other oxime carbamates (e.g., methomyl) have degradates which show no insecticidal activity, have low to negligible ecotoxicity and mammalian toxicity relative to the parent, and are normally nondetectable in crops. Therefore, the residue definition may include the parent oxime carbamate (e.g., methomyl) or parent and metabolites (e.g., aldicarb and its sulfoxide and sulfone metabolites). The tolerance or maximum residue limit (MRL) of pesticides on any food commodity is based on the highest residue concentration detected on mature crops at harvest or the LOQ of the method submitted for enforcement purposes if no detectable residues are found. For example, the tolerances of methomyl in US food commodities range from 0.1 to 6 mg kg for food items and up to 40 mg kg for feed items. ... 

Human toxicity values have not been established or have not been published. However, this agent is a powerful cholinesterase inhibitor. 

Although bicyclophosphates do not inhibit acetylcholinesterase, they exhibit a synergistic toxic effect with materials that do. Individuals who have had previous exposure to cholinesterase inhibitors such as nerve agents and commercial organophosphate or carbamate pesticides may be at a greater risk from exposure to bicyclophosphates. 

Carbachol, topical cholinesterase inhibitors, and oral CAIs (e.g., aceta-zolamide) are used as last-resort options after failure of less toxic options. 

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