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Inhibition acetyl cholinesterase

In addition to battlefield trauma, there is also the risk of exposure to chemical weapons such as the nerve agents, notably the organophosphorus gases (soman, sarin, VX, tabun) [6]. Organophosphorus toxicity arises largely from their ability to irreversibly inhibit acetyl-cholinesterases, leading to effects associated with peripheral acetyl-choline accumulation (muscarinic syndrome) such as meiosis, profuse sweating, bradychardia, bronchioconstriction, hypotension, and diarrhoea. Central nervous system effects include anxiety, restlessness, confusion, ataxia, tremors. [Pg.118]

H-4) Nerve gas. It is not necessary to cripple the Main Powerhouse in order to poison someone. Nerve gas, as well as organophosphate insecticides, inhibit acetyl cholinesterase (AOiE), an enzyme important in the degradation of acetylcholine to choline. This can cause paralysis through inhibiting AChE at the junction between... [Pg.52]

Organophosphate and carbamate pesticides are potent inhibitors of the enzyme cholinesterase. The inhibition of cholinesterase activity by the pesticide leads to the formation of stable covalent intermediates such as phosphoryl-enzyme complexes, which makes the hydrolysis of the substrate very slow. Both organophosphorus and carbamate pesticides can react with AChE in the same manner because the acetylation of the serine residue at the catalytic center is analogous to phosphorylation and carbamylation. Carbamated enzyme can restore its catalytic activity more rapidly than phosphorylated enzyme [17,42], Kok and Hasirci [43] reported that the total anti-cholinesterase activity of binary pesticide mixtures was lower than the sum of the individual inhibition values. [Pg.58]

The effect of Li+ upon the synthesis and release of acetylcholine in the brain is equivocal Li+ is reported to both inhibit and stimulate the synthesis of acetylcholine (reviewed by Wood et al. [162]). Li+ appears to have no effect on acetyl cholinesterase, the enzyme which catalyzes the hydrolysis of acetylcholine [163]. It has also been observed that the number of acetylcholine receptors in skeletal muscle is decreased by Li+ [164]. In the erythrocytes of patients on Li+, the concentration of choline is at least 10-fold higher than normal and the transport of choline is reduced [165] the effect of Li+ on choline transport in other cells is not known. A Li+-induced inhibition of either choline transport and/or the synthesis of acetylcholine could be responsible for the observed accumulation of choline in erythrocytes. This choline is probably derived from membrane phosphatidylcholine which is reportedly decreased in patients on Li+ [166],... [Pg.30]

Dose-effect dependence is shared by many OPC in both the acute and chronic tests. The higher dose of an anti-cholinesterase substance, the higher degree of both acetyl cholinesterase (AChE) inhibition in neural tissue and intoxication evidence. [Pg.102]

The UK Pesticide Safety Directorate (PSD) has decided to use the TEF approach for assessment of combined risk from exposure to mixtures of acetyl cholinesterase inhibitors (organophosphate (OP) compounds and carbamates) (PSD 1999). Despite clear differences in the action of carbamates and OP compounds, the index compounds selected for all acetyl cholinesterase inhibitors were either aldicarb (carbamate) or chlorpyrifos (OP). The POD for determining relative potency was predetermined as the dose level that produced 20% inhibition of red blood cell cholinesterase in a 90-day dietary study in rats. [Pg.388]

Methods for Determining Biomarkers of Exposure and Effect. Section 2.6.1 reported on biomarkers used to identify or quantify exposure to diazinon. Some methods for the detection of the parent compound in biological samples were described above. The parent chemical is quickly metabolized so the determination of metabolites can also serve as biomarkers of exposure. The most specific biomarkers will be those metabolites related to 2-isopropyl-6-methyl-4-hydroxypyrimidine. A method for this compound and 2-(r-hydroxy-l -methyl)-ethyl-6-methyl-4-hydroxypyrimidine in dog urine has been described by Lawrence and Iverson (1975) with reported sensitivities in the sub-ppm range. Other metabolites most commonly detected are 0,0-diethylphosphate and 0,0-diethylphosphorothioate, although these compounds are not specific for diazinon as they also arise from other diethylphosphates and phosphorothioates (Drevenkar et al. 1993 Kudzin et al. 1991 Mount 1984 Reid and Watts 1981 Vasilic et al. 1993). Another less specific marker of exposure is erythrocyte acetyl cholinesterase, an enzyme inhibited by insecticidal organophosphorus compounds (see Chapter 2). Methods for the diazinon-specific hydroxypyrimidines should be updated and validated for human samples. Rapid, simple, and specific methods should be sought to make assays readily available to the clinician. Studies that relate the exposure concentration of diazinon to the concentrations of these specific biomarkers in blood or urine would provide a basis for the interpretation of such biomarker data. [Pg.179]

Anthelmintic drugs can act in a variety of ways, by influencing the metabolism of the parasite (e.g. dismption of glucose and glycogen metabolism) or neuromuscular effects (e.g. inhibition of acetyl cholinesterase - organo-phosphates). The compounds are usually administered to animals orally, by injections, as feed additives or in the form of pour-on preparations. [Pg.126]

Mixed model with concentration addition for all compounds that share 1 mode of action In current practice (e.g., Traas et al. 2002 Mulder et al. 2004 De Zwart and Posthuma 2005), concentration addition is also applied to mixtures of nonnarcotic compounds with the same mode of action, such as photosynthesis inhibition or acetyl-cholinesterase inhibition. The protocol is shown in Figure 5.2. [Pg.163]

The synthesis, toxicity, neuroprotection, and human acetyl-cholinesterase/butyrylcholinesterase inhibition properties of ft-naphthotacrinesl-14 have been reported [176]. p-Naphthotacrines 1-14 showed lower toxicity than tacrine. [Pg.397]

The mode of action of physostigmine involves an inhibition of the enzyme acetyl cholinesterase. Physostigmine is an alkaloid with tertiary nitrogen, which gives a good penetration through the cornea. [Pg.129]

With an excessive, single exposure, the result will be either a systemic pesticide poisoning or a topical lesion frequently observed on the skin or in the eyes. Since most acute intoxications are from the carbamate and organoposphate insecticides, the systemic manifestations are cholinergic and are due to the inhibition of acetyl cholinesterase and the resultant accumulation of the neurotransmitter acetylcholine, at the synapse. Topical effects, in contrast, either are the result of the irritant properties of the chemicals in the formulation or have an allergenic basis for their occurrence (3). However, topical effects are not necessarily exclusively the result of exposure to the active ingredient in the formulation but may result from a reaction to one or more inerts as well. [Pg.129]

With a rise in dose of the substance entered, effect grows up irrespective of route of its entry into the organism. The higher dose of an anti-cholinesterase substance, the higher degree of both acetyl cholinesterase (AChE) inhibition in neural tissue and intoxication evidence. At high levels of exposure, any dose-effect dependence can be described by an exponential curve. The dynamics of efficient doses of lower level shows different variations, which however always come to either S-like or exponential curves [5, 8, 13],... [Pg.157]

The toxicant may react with an enzyme or a transport protein and inhibit its normal function. Enzymes may be inhibited by a compound that has a similar, but not identical structure as the true substrate instead of being processed, it blocks the enzyme. Typical toxicants of this kind are the carbamates and the organophosphorus insecticides that inhibit the enzyme acetyl cholinesterase. Some extremely efficient herbicides that inhibit enzymes important for amino acid synthesis in plants, e.g., glyphosate and glufosinate, are other good examples in this category. [Pg.16]

The effect of a number of oximes derived from pyridines on rat-brain acetyl cholinesterase which had been inactivated by isopropyl methyl-phosphonofluoridate has been studied, the most effective at restoring enzymic activity being (75). Acetyl cholinesterase is also inhibited by aryl... [Pg.173]

Benslama et al. (2004) have reported two unnsnal cases of malathion poisoning with a rare-type of complication from intermediate syndrome arising 2 to 4 days after the onset of cholinergic effects. The symptoms were respiratory paresis with difficulties of weaning from assisted respiratory, deficit of proximal limbs, neck flexors and cranial nerves. The authors attributed this syndrome to prolonged inhibition of acetyl-cholinesterases and not to any mnscnlar fiber s necrosis. [Pg.802]

Various pharmaceuticals and biocides are derived from benzo[b]thiophene, being bioisosteric with naphthalene and indole. Mobam (16, 4-(N-methylcarbamoyl)benzo[b]-thiophene) is an insecticide which is as effective as carbaryl (17). Both compounds inhibit the enzyme acetyl cholinesterase. [Pg.103]


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See also in sourсe #XX -- [ Pg.1012 ]

See also in sourсe #XX -- [ Pg.1012 ]




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Acetyl-cholinesterase, pesticide inhibition

Cholinesterase

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