Drugs used to reverse the inactivation of cholinesterase caused by organophosphates or sulfonates. They are an important component of therapy in agricultural, industrial, and military poisonings by organophosphates and sulfonates.
An organothiophosphate insecticide.
Cholinesterase reactivator used as an antidote in alkyl phosphate poisoning.
Cholinesterases are a group of enzymes that catalyze the hydrolysis of acetylcholine and other choline esters, playing crucial roles in the termination of impulse transmission at cholinergic synapses and neuro-muscular junctions, and in the metabolism of certain drugs and toxic substances.
Cholinesterase reactivator occurring in two interchangeable isomeric forms, syn and anti.
Drugs that inhibit cholinesterases. The neurotransmitter ACETYLCHOLINE is rapidly hydrolyzed, and thereby inactivated, by cholinesterases. When cholinesterases are inhibited, the action of endogenously released acetylcholine at cholinergic synapses is potentiated. Cholinesterase inhibitors are widely used clinically for their potentiation of cholinergic inputs to the gastrointestinal tract and urinary bladder, the eye, and skeletal muscles; they are also used for their effects on the heart and the central nervous system.
Compounds that contain the radical R2C=N.OH derived from condensation of ALDEHYDES or KETONES with HYDROXYLAMINE. Members of this group are CHOLINESTERASE REACTIVATORS.
Various salts of a quaternary ammonium oxime that reconstitute inactivated acetylcholinesterase, especially at the neuromuscular junction, and may cause neuromuscular blockade. They are used as antidotes to organophosphorus poisoning as chlorides, iodides, methanesulfonates (mesylates), or other salts.
An enzyme that catalyzes the hydrolysis of ACETYLCHOLINE to CHOLINE and acetate. In the CNS, this enzyme plays a role in the function of peripheral neuromuscular junctions. EC 3.1.1.7.
An organophosphorus ester compound that produces potent and irreversible inhibition of cholinesterase. It is toxic to the nervous system and is a chemical warfare agent.
Carbon-containing phosphoric acid derivatives. Included under this heading are compounds that have CARBON atoms bound to one or more OXYGEN atoms of the P(=O)(O)3 structure. Note that several specific classes of endogenous phosphorus-containing compounds such as NUCLEOTIDES; PHOSPHOLIPIDS; and PHOSPHOPROTEINS are listed elsewhere.
An organophosphate cholinesterase inhibitor that is used as a pesticide.
Agents counteracting or neutralizing the action of POISONS.
Pyridinium compounds are organic salts formed when pyridine, a basic heterocyclic organic compound, reacts with acids, resulting in a positively charged nitrogen atom surrounded by aromatic rings.
Chemicals that are used to cause the disturbance, disease, or death of humans during WARFARE.
An aspect of cholinesterase (EC 3.1.1.8).
Poisoning due to exposure to ORGANOPHOSPHORUS COMPOUNDS, such as ORGANOPHOSPHATES; ORGANOTHIOPHOSPHATES; and ORGANOTHIOPHOSPHONATES.
Organic compounds that contain phosphorus as an integral part of the molecule. Included under this heading is broad array of synthetic compounds that are used as PESTICIDES and DRUGS.
Compounds which restore enzymatic activity by removing an inhibitory group bound to the reactive site of the enzyme.
A mercaptocholine used as a reagent for the determination of CHOLINESTERASES. It also serves as a highly selective nerve stain.
An organochlorophosphate cholinesterase inhibitor that is used as an insecticide for the control of flies and roaches. It is also used in anthelmintic compositions for animals. (From Merck, 11th ed)
An aspect of cholinesterases.
Phenyl esters of carbamic acid or of N-substituted carbamic acids. Structures are similar to PHENYLUREA COMPOUNDS with a carbamate in place of the urea.
An organothiophosphate cholinesterase inhibitor that is used as an insecticide and as an acaricide.
A cholinesterase inhibitor used in the treatment of myasthenia gravis and to reverse the effects of muscle relaxants such as gallamine and tubocurarine. Neostigmine, unlike PHYSOSTIGMINE, does not cross the blood-brain barrier.
Aryl CYCLOPENTANES that are a reduced (protonated) form of INDENES.
A local anesthetic of the amide type now generally used for surface anesthesia. It is one of the most potent and toxic of the long-acting local anesthetics and its parenteral use is restricted to spinal anesthesia. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1006)
A cholinesterase inhibitor that crosses the blood-brain barrier. Tacrine has been used to counter the effects of muscle relaxants, as a respiratory stimulant, and in the treatment of Alzheimer's disease and other central nervous system disorders.
A cholinesterase inhibitor that is rapidly absorbed through membranes. It can be applied topically to the conjunctiva. It also can cross the blood-brain barrier and is used when central nervous system effects are desired, as in the treatment of severe anticholinergic toxicity.
A benzazepine derived from norbelladine. It is found in GALANTHUS and other AMARYLLIDACEAE. It is a cholinesterase inhibitor that has been used to reverse the muscular effects of GALLAMINE TRIETHIODIDE and TUBOCURARINE and has been studied as a treatment for ALZHEIMER DISEASE and other central nervous system disorders.
A cholinesterase inhibitor that is used as an organothiophosphorus insecticide.
N,N',N'',N'''-Tetraisopropylpyrophosphamide. A specific inhibitor of pseudocholinesterases. It is commonly used experimentally to determine whether pseudo- or acetylcholinesterases are involved in an enzymatic process.
Pesticides designed to control insects that are harmful to man. The insects may be directly harmful, as those acting as disease vectors, or indirectly harmful, as destroyers of crops, food products, or textile fabrics.
A highly toxic cholinesterase inhibitor that is used as an acaricide and as an insecticide.
Compounds containing carbon-phosphorus bonds in which the phosphorus component is also bonded to one or more sulfur atoms. Many of these compounds function as CHOLINERGIC AGENTS and as INSECTICIDES.
An organophosphorus insecticide that inhibits ACETYLCHOLINESTERASE.
A quaternary skeletal muscle relaxant usually used in the form of its bromide, chloride, or iodide. It is a depolarizing relaxant, acting in about 30 seconds and with a duration of effect averaging three to five minutes. Succinylcholine is used in surgical, anesthetic, and other procedures in which a brief period of muscle relaxation is called for.
A cholinesterase inhibitor with a slightly longer duration of action than NEOSTIGMINE. It is used in the treatment of myasthenia gravis and to reverse the actions of muscle relaxants.
An organothiophosphate cholinesterase inhibitor that is used as an insecticide.
A carbamate insecticide and parasiticide. It is a potent anticholinesterase agent belonging to the carbamate group of reversible cholinesterase inhibitors. It has a particularly low toxicity from dermal absorption and is used for control of head lice in some countries.
A carbamate insecticide with anticholinesterase activity.
Derivatives of carbamic acid, H2NC(=O)OH. Included under this heading are N-substituted and O-substituted carbamic acids. In general carbamate esters are referred to as urethanes, and polymers that include repeating units of carbamate are referred to as POLYURETHANES. Note however that polyurethanes are derived from the polymerization of ISOCYANATES and the singular term URETHANE refers to the ethyl ester of carbamic acid.
A sulfur-containing analog of butyrylcholine which is hydrolyzed by butyrylcholinesterase to butyrate and thiocholine. It is used as a reagent in the determination of butyrylcholinesterase activity.
An organophosphorus compound that inhibits cholinesterase. It causes seizures and has been used as a chemical warfare agent.
Events that overwhelm the resources of local HOSPITALS and health care providers. They are likely to impose a sustained demand for HEALTH SERVICES rather than the short, intense peak customary with smaller scale disasters.

A case of aldicarb poisoning: a possible murder attempt. (1/98)

A couple showing signs of cholinergic crisis was admitted to the hospital. Analyses with high-performance liquid chromatography and gas chromatography-mass spectrometry conducted on serum, urine, and stomach contents that were collected few hours after first symptoms showed the presence of aldicarb, which is the most potent carbamate insecticide on the market. A murder attempt was suspected because the patients showed the first signs some minutes after drinking coffee upon returning home and no commercial products containing aldicarb were found in the house. Because of the reversibility of inhibition of acetylcholinesterase, the patients recovered after treatment with atropine and toxogonin. They left the hospital after 12 days. To our knowledge, the serum concentrations of aldicarb reported in this paper are the highest reported for a nonfatal case.  (+info)

Positive inotropic effect of insulin-like growth factor-1 on normal and failing cardiac myocytes. (2/98)

OBJECTIVE: The acute administration of growth hormone (GH) or insulin-like growth factor-1 (IGF-1) improves cardiac performance, possibly contributing to the beneficial effects of GH therapy on heart failure (HF). GH can induce the production of IGF-1 and thus the actions of GH may be mediated through its IGF-1 induction. However, these effects have not yet been demonstrated in failing hearts and the cellular basis of GH or IGF-1-induced inotropic effects remains unknown. We examined the direct effects of GH and IGF-1 on the contractile function and intracellular calcium ([Ca2+]i) homeostasis in normal and failing myocytes. METHODS: To determine whether GH and IGF-1 have a direct effect on myocardial contractility and whether the GH/IGF-1-induced effect was the results of changes in Ca2+ activation, cell shortening and [Ca2+]i transient were simultaneously measured in the left ventricular myocyte preparations, isolated from normal and rapid pacing-induced HF dogs. RESULTS: Basal shortening of HF myocytes was reduced by 64% (p < 0.01). In normal and HF myocytes, GH (0.4-40 x 10(-3) IU/ml) had no effect on either cell shortening or [Ca2+]i transients. In normal myocytes, IGF-1 exerted a positive inotropic effect in a time- and dose-dependent manner (25-500 ng/ml), associated with a parallel increase of [Ca2+]i transient amplitude. IGF-1 increased the shortening magnitude in normal (121 +/- 5% increase from baseline, p < 0.05) and HF (118 +/- 4% increase from baseline, p < 0.05) myocytes. It also increased [Ca2+]i transient amplitude in normal and HF cells by 124 +/- 4 and 125 +/- 7%, respectively. The percent increase of cell shortening and [Ca2+]i transient amplitude was comparable between normal and HF myocytes. Furthermore, IGF-1 did not shift the trajectory of the relaxation phase in the phase-plane plots of cell length vs. [Ca2+]i, indicating that it did not change myofilament Ca2+ sensitivity. CONCLUSIONS: In both normal and HF conditions, IGF-1 exerted an acute direct positive inotropic effect in adult cardiac myocytes by increasing the availability of [Ca2+]i to the myofilaments, possibly explaining the beneficial effect of GH on HF.  (+info)

Inhibitory effect of 2,3-butanedione monoxime (BDM) on Na(+)/Ca(2+) exchange current in guinea-pig cardiac ventricular myocytes. (3/98)

1. The effect of 2,3-butanedione monoxime (BDM), a 'chemical phosphatase', on Na(+)/Ca(2+) exchange current (I(NCX)) was investigated using the whole-cell voltage-clamp technique in single guinea-pig cardiac ventricular myocytes and in CCL39 fibroblast cells expressing canine NCX1. 2. I(NCX) was identified as a current sensitive to KB-R7943, a relatively selective NCX inhibitor, at 140 mM Na(+) and 2 mM Ca(2+) in the external solution and 20 mM Na(+) and 433 nM free Ca(2+) in the pipette solution. 3. In guinea-pig ventricular cells, BDM inhibited I(NCX) in a concentration-dependent manner. The IC(50) value was 2.4 mM with a Hill coefficients of 1. The average time for 50% inhibition by 10 mM BDM was 124+/-31 s (n=5). 4. The effect of BDM was not affected by 1 microM okadaic acid in the pipette solution, indicating that the inhibition was not via activation of okadaic acid-sensitive protein phosphatases. 5. Intracellular trypsin treatment via the pipette solution significantly suppressed the inhibitory effect of BDM, implicating an intracellular site of action of BDM. 6. PAM (pralidoxime), another oxime compound, also inhibited I(NCX) in a manner similar to BDM. 7. Isoprenaline at 50 microM and phorbol 12-myristate 13-acetate (PMA) at 8 microM did not reverse the inhibition of I(NCX) by BDM. 8. BDM inhibited I(NCX) in CCL39 cells expressing NCX1 and in its mutant in which its three major phosphorylatable serine residues were replaced with alanines. 9. We conclude that BDM inhibits I(NCX) but the mechanism of inhibition is not by dephosphorylation of the Na(+)/Ca(2+) exchanger as a 'chemical phosphatase'.  (+info)

Force spectroscopy between acetylcholine and single acetylcholinesterase molecules and the effects of inhibitors and reactivators studied by atomic force microscopy. (4/98)

Force spectroscopy between a single acetylcholinesterase (AChE) molecule and its natural substrates was performed, and the effects of inhibitors and reactivators on the force spectrum were studied with atomic force microscopy (AFM). The force spectrum between normal AChE and its substrates had its special shape. Inhibitors, which inhibit AChE by occupying the active center of the enzyme, could change the force spectrum shape noticeably. Reactivators, which reactivate the inhibited AChE by pulling the inhibitor off the active center of the enzyme, could make the normal shape of force spectrum reappear. This meant the shape features of the force spectrum could be used as a good index to observe the time course of the interactions between a single AChE molecule and its special inhibitors and reactivators in real time. The results of the real-time observation demonstrated that the inhibition times of soman and sarin on AChE were longer than 2 h and that of eserine, a reversible inhibitor of AChE, was 34 +/- 3 min. The reactivation time of HI-6 on soman-inhibited AChE was 6 +/- 2 min. These results indicated that AFM was a useful tool in pharmacology and toxicology, and could reveal time information of the interactions between AChE and its ligands.  (+info)

Cholinesterase inhibition by aluminium phosphide poisoning in rats and effects of atropine and pralidoxime chloride. (5/98)

AIM: To investigate the cholinesterase inhibition and effect of atropine and pralidoxime (PAM) treatment on the survival time in the rat model of aluminium phosphide (AlP) poisoning. METHODS: The rats were treated with AlP (10 mg/kg; 5.55 x LD50; ig) and the survival time was noted. The effect of atropine (1 mg/kg, ip) and PAM (5 mg/kg, ip) was noted on the above. Atropine and PAM were administered 5 min after AlP. Plasma cholinesterase levels were measured spectrophotometrically in the control and AlP treated rats 30 min after administration. RESULTS: Treatment with atropine and PAM increased the survival time by 2.5 fold (1.4 h+/-0.3 h vs 3.4 h+/-2.5 h, P < 0.01) in 9 out of 15 animals and resulted in total survival of the 6 remaining animals. Plasma cholinesterase levels were inhibited by 47 %, (438+/-74) U/L in AlP treated rats as compared to control (840+/-90) U/L (P < 0.01). CONCLUSION: This preliminary study concludes that AlP poisoning causes cholinesterase inhibition and responds to treatment with atropine and PAM.  (+info)

Reactivation of immobilized acetyl cholinesterase in an amperometric biosensor for organophosphorus pesticide. (6/98)

Biosensors based on acetyl cholinesterase (AChE) inhibition have been known for monitoring of pesticides in food and water samples. However, strong inhibition of the enzyme is a major drawback in practical application of the biosensor which can be overcome by reactivation of the enzyme for repeated use. In the present study, enzyme reactivation by oximes was explored for this purpose. Two oximes viz., 1,1'-trimethylene bis 4-formylpyridinium bromide dioxime (TMB-4) and pyridine 2-aldoxime methiodide (2-PAM) were compared for the reactivation of the immobilized AChE. TMB-4 was found to be a more efficient reactivator under repeated use, retaining more than 60% of initial activity after 11 reuses, whereas in the case of 2-PAM, the activity retention dropped to less than 50% after only 6 reuses. Investigations also showed that reactivation must be effected within 10 min after each analysis to eliminate the ageing effect, which reduces the efficiency of reactivation.  (+info)

Myosin II is present in gastric parietal cells and required for lamellipodial dynamics associated with cell activation. (7/98)

Nonmuscle myosin II has been shown to participate in organizing the actin cytoskeleton in polarized epithelial cells. Vectorial acid secretion in cultured parietal cells involves translocation of proton pumps from cytoplasmic vesicular membranes to the apical plasma membrane vacuole with coordinated lamellipodial dynamics at the basolateral membrane. Here we identify nonmuscle myosin II in rabbit gastric parietal cells. Western blots with isoform-specific antibodies indicate that myosin IIA is present in both cytosolic and particulate membrane fractions whereas the IIB isoform is associated only with particulate fractions. Immunofluorescent staining demonstrates that myosin IIA is diffusely located throughout the cytoplasm of resting parietal cells. However, after stimulation, myosin IIA is rapidly redistributed to lamellipodial extensions at the cell periphery; virtually all the cytoplasmic myosin IIA joins the newly formed basolateral membrane extensions. 2,3-Butanedione monoximine (BDM), a myosin-ATPase inhibitor, greatly diminishes the lamellipodial dynamics elicited by stimulation and retains the pattern of myosin IIA cytoplasmic staining. However, BDM had no apparent effect on the stimulation associated redistribution of H,K-ATPase from a cytoplasmic membrane compartment to apical membrane vacuoles. The myosin light chain kinase inhibitor 1-(5-iodonaphthalene-1-sulfonyl)-1H-hexahydro-1,4-diazepine (ML-7) also did not alter the stimulation-associated recruitment of H,K-ATPase to apical membrane vacuoles, but unlike BDM it had relatively minor inhibitory effects on lamellipodial dynamics. We conclude that specific disruption of the basolateral actomyosin cytoskeleton has no demonstrable effect on recruitment of H,K-ATPase-rich vesicles into the apical secretory membrane. However, myosin II plays an important role in regulating lamellipodial dynamics and cortical actomyosin associated with parietal cell activation.  (+info)

Rational design of alkylene-linked bis-pyridiniumaldoximes as improved acetylcholinesterase reactivators. (8/98)

To improve the potency of 2-pralidoxime (2-PAM) for treating organophosphate poisoning, we dimerized 2-PAM and its analogs according to Wilson's pioneering work and the 3D structure of human acetylcholinesterase (hAChE) inactivated by isoflurophate. 1,7-Heptylene-bis-N,N'-syn-2-pyridiniumaldoxime, the most potent of the alkylene-linked dimeric reactivators, was readily synthesized using bistriflate and is 100 times more potent than 2-PAM in reactivating hAChE poisoned by isoflurophate. Experimental and computational studies confirm that 2-PAM in its biologically active form adopts the syn-I configuration. Further, they suggest that the improved performance of dimeric oximes is conferred by two-site binding with one oxime pointing toward the diisopropyl ester at the catalytic site of hAChE and the other anchored at the peripheral site. This type of binding may induce a conformational change in the acyl pocket loop which modulates the catalytic site via a domino effect.  (+info)

Cholinesterase reactivators are a type of medication used to reverse the effects of certain types of poisoning, particularly organophosphate and carbamate pesticides, as well as nerve agents. These chemicals work by inhibiting the enzyme acetylcholinesterase, which normally breaks down the neurotransmitter acetylcholine in the body. This can lead to an overaccumulation of acetylcholine and result in symptoms such as muscle weakness, seizures, and respiratory failure.

Cholinesterase reactivators, also known as oximes, work by reactivating the inhibited enzyme and allowing it to resume its normal function. The most commonly used cholinesterase reactivator is pralidoxime (2-PAM), which is often administered in combination with atropine to treat organophosphate poisoning.

It's important to note that cholinesterase reactivators are not effective against all types of nerve agents or pesticides, and their use should be determined by a medical professional based on the specific type of poisoning involved. Additionally, these medications can have side effects and should only be administered under medical supervision.

Disulfoton is a type of organophosphate pesticide that is used to control a variety of insects in agricultural settings. It functions as a cholinesterase inhibitor, disrupting the normal functioning of the nervous system in insects and leading to their death. However, disulfoton can also have toxic effects on humans and other mammals if ingested, inhaled, or absorbed through the skin. Therefore, it is important to use appropriate safety measures when handling this chemical.

The medical definition of Disulfoton is:

A colorless to light brown oily liquid organophosphate insecticide and acaricide. It is used for control of soil-inhabiting pests on a wide variety of crops, including corn, soybeans, potatoes, and ornamentals. Disulfoton is also used as a termiticide and a molluscicide. It acts by inhibition of cholinesterase. Exposure may occur through ingestion, inhalation, or skin absorption. Symptoms of exposure include nausea, vomiting, diarrhea, abdominal cramps, headache, dizziness, and tightness in the chest. Severe exposure can lead to respiratory failure, convulsions, unconsciousness, and death. Disulfoton is considered a highly toxic compound.

Trimedoxime is an antidote drug that is used to treat poisoning by organophosphate chemicals, which are commonly found in pesticides and nerve agents. It works by reactivating the acetylcholinesterase enzyme, which is inhibited by these toxic compounds, thereby restoring the normal functioning of the nervous system.

Medically, trimedoxime is classified as an oxime, a type of compound that can reverse the effects of organophosphate poisoning. It is often used in combination with atropine, another antidote drug that blocks the action of acetylcholine, a neurotransmitter that accumulates in the body due to organophosphate poisoning.

It's important to note that trimedoxime should only be administered under medical supervision and in accordance with established protocols for treating organophosphate poisoning. Improper use of this drug can lead to serious adverse effects.

Cholinesterases are a group of enzymes that play an essential role in the nervous system by regulating the transmission of nerve impulses. They work by breaking down a type of chemical messenger called acetylcholine, which is released by nerves to transmit signals to other nerves or muscles.

There are two main types of cholinesterases: acetylcholinesterase (AChE) and butyrylcholinesterase (BChE). AChE is found primarily in the nervous system, where it rapidly breaks down acetylcholine to terminate nerve impulses. BChE, on the other hand, is found in various tissues throughout the body, including the liver and plasma, and plays a less specific role in breaking down various substances, including some drugs and toxins.

Inhibition of cholinesterases can lead to an accumulation of acetylcholine in the synaptic cleft, which can result in excessive stimulation of nerve impulses and muscle contractions. This effect is exploited by certain medications used to treat conditions such as myasthenia gravis, Alzheimer's disease, and glaucoma, but can also be caused by exposure to certain chemicals or toxins, such as organophosphate pesticides and nerve agents.

Obidoxime chloride is a medication that belongs to the class of drugs known as oximes. It is used as an antidote for nerve agent and organophosphate poisoning. Obidoxime works by reactivating the inhibited acetylcholinesterase enzyme, which is essential for normal functioning of the nervous system. This enzyme can be inhibited by nerve agents and organophosphates, leading to an overstimulation of the nervous system that can result in symptoms such as muscle weakness, seizures, respiratory failure, and death.

Obidoxime is administered intravenously and works by breaking down the bond between the nerve agent or organophosphate and the acetylcholinesterase enzyme, allowing the enzyme to function normally again. It is important to note that obidoxime should be administered as soon as possible after exposure to a nerve agent or organophosphate in order to be effective.

It's important to mention that Obidoxime Chloride is not used frequently and only in specific situations, it requires medical supervision and administration by trained healthcare professionals.

Cholinesterase inhibitors are a class of drugs that work by blocking the action of cholinesterase, an enzyme that breaks down the neurotransmitter acetylcholine in the body. By inhibiting this enzyme, the levels of acetylcholine in the brain increase, which can help to improve symptoms of cognitive decline and memory loss associated with conditions such as Alzheimer's disease and other forms of dementia.

Cholinesterase inhibitors are also used to treat other medical conditions, including myasthenia gravis, a neuromuscular disorder that causes muscle weakness, and glaucoma, a condition that affects the optic nerve and can lead to vision loss. Some examples of cholinesterase inhibitors include donepezil (Aricept), galantamine (Razadyne), and rivastigmine (Exelon).

It's important to note that while cholinesterase inhibitors can help to improve symptoms in some people with dementia, they do not cure the underlying condition or stop its progression. Side effects of these drugs may include nausea, vomiting, diarrhea, and increased salivation. In rare cases, they may also cause seizures, fainting, or cardiac arrhythmias.

Oximes are a class of chemical compounds that contain the functional group =N-O-, where two organic groups are attached to the nitrogen atom. In a clinical context, oximes are used as antidotes for nerve agent and pesticide poisoning. The most commonly used oxime in medicine is pralidoxime (2-PAM), which is used to reactivate acetylcholinesterase that has been inhibited by organophosphorus compounds, such as nerve agents and certain pesticides. These compounds work by forming a bond with the phosphoryl group of the inhibited enzyme, allowing for its reactivation and restoration of normal neuromuscular function.

Pralidoxime compounds are a type of antidote used to treat poisoning from organophosphate nerve agents and pesticides. These compounds work by reactivating the acetylcholinesterase enzyme, which is inhibited by organophosphates. This helps to restore the normal functioning of the nervous system and can save lives in cases of severe poisoning.

Pralidoxime is often used in combination with atropine, another antidote that blocks the effects of excess acetylcholine at muscarinic receptors. Together, these compounds can help to manage the symptoms of organophosphate poisoning and prevent long-term neurological damage.

It is important to note that pralidoxime must be administered as soon as possible after exposure to organophosphates, as its effectiveness decreases over time. This makes rapid diagnosis and treatment crucial in cases of suspected nerve agent or pesticide poisoning.

Acetylcholinesterase (AChE) is an enzyme that catalyzes the hydrolysis of acetylcholine (ACh), a neurotransmitter, into choline and acetic acid. This enzyme plays a crucial role in regulating the transmission of nerve impulses across the synapse, the junction between two neurons or between a neuron and a muscle fiber.

Acetylcholinesterase is located in the synaptic cleft, the narrow gap between the presynaptic and postsynaptic membranes. When ACh is released from the presynaptic membrane and binds to receptors on the postsynaptic membrane, it triggers a response in the target cell. Acetylcholinesterase rapidly breaks down ACh, terminating its action and allowing for rapid cycling of neurotransmission.

Inhibition of acetylcholinesterase leads to an accumulation of ACh in the synaptic cleft, prolonging its effects on the postsynaptic membrane. This can result in excessive stimulation of cholinergic receptors and overactivation of the cholinergic system, which may cause a range of symptoms, including muscle weakness, fasciculations, sweating, salivation, lacrimation, urination, defecation, bradycardia, and bronchoconstriction.

Acetylcholinesterase inhibitors are used in the treatment of various medical conditions, such as Alzheimer's disease, myasthenia gravis, and glaucoma. However, they can also be used as chemical weapons, such as nerve agents, due to their ability to disrupt the nervous system and cause severe toxicity.

Sarin is a potent and deadly nerve agent, a type of organic compound called a phosphoro-organic fluid. It is a colorless, odorless, and tasteless liquid, which is also known as GB. Sarin is a human-made chemical warfare agent that is considered a weapon of mass destruction and is banned under the Chemical Weapons Convention of 1993.

Sarin works by inhibiting the enzyme acetylcholinesterase, which is responsible for breaking down the neurotransmitter acetylcholine in the body. This leads to an overaccumulation of acetylcholine at the neuromuscular junctions and synapses, causing uncontrolled muscle contractions, paralysis, respiratory failure, and ultimately death if not treated promptly.

Exposure to Sarin can occur through inhalation, skin contact, or ingestion. Symptoms of exposure include runny nose, tightness in the chest, difficulty breathing, nausea, vomiting, diarrhea, blurred vision, and confusion. Immediate medical attention is required for anyone exposed to Sarin, as antidotes such as atropine and pralidoxime can be administered to counteract its effects.

Organophosphates are a group of chemicals that include insecticides, herbicides, and nerve gases. They work by inhibiting an enzyme called acetylcholinesterase, which normally breaks down the neurotransmitter acetylcholine in the synapse between nerves. This leads to an overaccumulation of acetylcholine, causing overstimulation of the nervous system and resulting in a wide range of symptoms such as muscle twitching, nausea, vomiting, diarrhea, sweating, confusion, and potentially death due to respiratory failure. Organophosphates are highly toxic and their use is regulated due to the risks they pose to human health and the environment.

Paraoxon is the active metabolite of the organophosphate insecticide parathion. It functions as an acetylcholinesterase inhibitor, which means it prevents the breakdown of the neurotransmitter acetylcholine in the synaptic cleft. This leads to an accumulation of acetylcholine and overstimulation of cholinergic receptors, causing a variety of symptoms such as muscle weakness, increased salivation, sweating, lacrimation, nausea, vomiting, and potentially fatal respiratory failure.

Paraoxon is also used in research and diagnostic settings to measure acetylcholinesterase activity. It can be used to determine the degree of inhibition of this enzyme by various chemicals or toxins, including other organophosphate compounds.

An antidote is a substance that can counteract the effects of a poison or toxin. It works by neutralizing, reducing, or eliminating the harmful effects of the toxic substance. Antidotes can be administered in various forms such as medications, vaccines, or treatments. They are often used in emergency situations to save lives and prevent serious complications from poisoning.

The effectiveness of an antidote depends on several factors, including the type and amount of toxin involved, the timing of administration, and the individual's response to treatment. In some cases, multiple antidotes may be required to treat a single poisoning incident. It is important to note that not all poisons have specific antidotes, and in such cases, supportive care and symptomatic treatment may be necessary.

Examples of common antidotes include:

* Naloxone for opioid overdose
* Activated charcoal for certain types of poisoning
* Digoxin-specific antibodies for digoxin toxicity
* Fomepizole for methanol or ethylene glycol poisoning
* Dimercaprol for heavy metal poisoning.

Pyridinium compounds are organic salts that contain a positively charged pyridinium ion. Pyridinium is a type of cation that forms when pyridine, a basic heterocyclic organic compound, undergoes protonation. The nitrogen atom in the pyridine ring accepts a proton (H+) and becomes positively charged, forming the pyridinium ion.

Pyridinium compounds have the general structure of C5H5NH+X-, where X- is an anion or negatively charged ion. These compounds are often used in research and industry, including as catalysts, intermediates in chemical synthesis, and in pharmaceuticals. Some pyridinium compounds have been studied for their potential therapeutic uses, such as in the treatment of bacterial infections or cancer. However, it is important to note that some pyridinium compounds can also be toxic or reactive, so they must be handled with care.

Chemical warfare agents are defined as chemical substances that are intended or have the capability to cause death, injury, temporary incapacitation, or sensory irritation through their toxic properties when deployed in a military theater. These agents can be in gaseous, liquid, or solid form and are typically categorized based on their physiological effects. Common categories include nerve agents (e.g., sarin, VX), blister agents (e.g., mustard gas), choking agents (e.g., phosgene), blood agents (e.g., cyanide), and incapacitating agents (e.g., BZ). The use of chemical warfare agents is prohibited by international law under the Chemical Weapons Convention.

Butyrylcholinesterase (BChE) is an enzyme that catalyzes the hydrolysis of esters of choline, including butyrylcholine and acetylcholine. It is found in various tissues throughout the body, including the liver, brain, and plasma. BChE plays a role in the metabolism of certain drugs and neurotransmitters, and its activity can be inhibited by certain chemicals, such as organophosphate pesticides and nerve agents. Elevated levels of BChE have been found in some neurological disorders, while decreased levels have been associated with genetic deficiencies and liver disease.

Organophosphate (OP) poisoning refers to the toxic effects that occur after exposure to organophosphate compounds, which are commonly used as pesticides, nerve agents, and plasticizers. These substances work by irreversibly inhibiting acetylcholinesterase, an enzyme that breaks down the neurotransmitter acetylcholine in the nervous system. As a result, excessive accumulation of acetylcholine leads to overstimulation of cholinergic receptors, causing a wide range of symptoms.

The severity and type of symptoms depend on the dose, duration, and route of exposure (inhalation, ingestion, or skin absorption). The primary manifestations of organophosphate poisoning are:

1. Muscarinic effects: Excess acetylcholine at muscarinic receptors in the parasympathetic nervous system results in symptoms such as narrowed pupils (miosis), increased salivation, lacrimation, sweating, bronchorrhea (excessive respiratory secretions), diarrhea, bradycardia (decreased heart rate), and hypotension.
2. Nicotinic effects: Overstimulation of nicotinic receptors at the neuromuscular junction leads to muscle fasciculations, weakness, and paralysis. This can also cause tachycardia (increased heart rate) and hypertension.
3. Central nervous system effects: OP poisoning may result in headache, dizziness, confusion, seizures, coma, and respiratory depression.

Treatment for organophosphate poisoning includes decontamination, supportive care, and administration of antidotes such as atropine (to block muscarinic effects) and pralidoxime (to reactivate acetylcholinesterase). Delayed treatment can lead to long-term neurological damage or even death.

Organophosphorus compounds are a class of chemical substances that contain phosphorus bonded to organic compounds. They are used in various applications, including as plasticizers, flame retardants, pesticides (insecticides, herbicides, and nerve gases), and solvents. In medicine, they are also used in the treatment of certain conditions such as glaucoma. However, organophosphorus compounds can be toxic to humans and animals, particularly those that affect the nervous system by inhibiting acetylcholinesterase, an enzyme that breaks down the neurotransmitter acetylcholine. Exposure to these compounds can cause symptoms such as nausea, vomiting, muscle weakness, and in severe cases, respiratory failure and death.

Enzyme reactivators are substances or compounds that restore the activity of an enzyme that has been inhibited or inactivated. This can occur due to various reasons such as exposure to certain chemicals, oxidation, or heavy metal ions. Enzyme reactivators work by binding to the enzyme and reversing the effects of the inhibitor or promoting the repair of any damage caused.

One example of an enzyme reactivator is methionine sulfoxide reductase (Msr), which can reduce oxidized methionine residues in proteins, thereby restoring their function. Another example is 2-phenylethynesulfonamide (PESNA), which has been shown to reactivate the enzyme parkinsonism-associated deglycase (DJ-1) that is mutated in some cases of familial Parkinson's disease.

It is important to note that not all enzyme inhibitors can be reversed by reactivators, and the development of specific reactivators for particular enzymes is an active area of research with potential therapeutic applications.

Thiocholine is not a medical term per se, but it is a chemical compound that has applications in the medical and biological fields. Thiocholine is the reduced form of thiochrome, which is a derivative of vitamin B1 (thiamine). It is often used as a reagent in biochemical assays to measure the activity of acetylcholinesterase, an enzyme that breaks down the neurotransmitter acetylcholine.

In this context, thiocholine iodide (S-[2-(hydroxyethyl)thio]ethan-1-oniuim iodide) is commonly used as a substrate for acetylcholinesterase. When the enzyme hydrolyzes thiocholine iodide, it produces thiocholine, which can be detected and quantified through its reaction with ferric chloride to form a colored complex. This assay is useful in diagnosing certain neurological conditions or monitoring the effectiveness of treatments that target the cholinergic system.

Trichlorfon is an organophosphate insecticide and acaricide. It is used to control a wide variety of pests, including flies, ticks, and mites in agriculture, livestock production, and public health. Trichlorfon works by inhibiting the enzyme acetylcholinesterase, which leads to an accumulation of the neurotransmitter acetylcholine and results in paralysis and death of the pest. It is important to note that trichlorfon can also have harmful effects on non-target organisms, including humans, and its use is regulated by various governmental agencies to minimize potential risks.

Pseudocholinesterase, also known as butyrylcholinesterase or plasma cholinesterase, is an enzyme found in the blood plasma. It is responsible for breaking down certain types of drugs and muscle relaxants that are used during general anesthesia, such as succinylcholine and mivacurium.

Pseudocholinesterase deficiency can lead to prolonged neuromuscular blockade and difficulty in reversing the effects of these muscle relaxants, which can result in respiratory complications and other adverse effects during or after surgery. This deficiency can be inherited or acquired due to various factors such as liver disease, malnutrition, or exposure to certain chemicals.

It is important to test the patient's pseudocholinesterase levels before administering succinylcholine or mivacurium to ensure that they have adequate enzyme activity to metabolize these drugs properly.

Phenylcarbamates are a group of organic compounds that contain a phenyl group (a functional group consisting of a six-carbon ring, with the formula -C6H5) bonded to a carbamate group (-NHCOO-). Carbamates are compounds that contain a carbonyl (>C=O) group bonded to a nitrogen atom that is also bonded to two organic substituents.

In the medical field, phenylcarbamates have been used as drugs for various purposes. For example, some phenylcarbamates have been used as anticonvulsants, while others have been investigated for their potential as anti-cancer agents. However, it is important to note that many phenylcarbamates also have toxic properties and must be used with caution.

One well-known example of a phenylcarbamate is phenytoin, an anticonvulsant medication used to treat seizures. Phenytoin works by slowing down the transmission of nerve impulses in the brain, which can help prevent or reduce the severity of seizures.

It's worth noting that while phenylcarbamates have been studied for their potential therapeutic uses, they are not a widely used class of drugs and further research is needed to fully understand their mechanisms of action and potential side effects.

Chlorpyrifos is a type of pesticide that belongs to the class of organophosphates. It works by inhibiting the enzyme acetylcholinesterase, which leads to an accumulation of the neurotransmitter acetylcholine and causes toxic effects in insects. Chlorpyrifos is used to control a wide variety of pests, including insects that infest crops, homes, and gardens. It is also used to protect wood from termites and other wood-boring insects.

Chlorpyrifos can be harmful to humans if it is ingested, inhaled, or comes into contact with the skin. Exposure to chlorpyrifos can cause a range of symptoms, including nausea, vomiting, headache, dizziness, and muscle twitching. In severe cases, it can lead to respiratory failure, convulsions, and even death. Chlorpyrifos has been linked to developmental problems in children, including reduced IQ and attention deficit disorder. As a result, the use of chlorpyrifos in residential settings has been restricted in many countries.

Neostigmine is a medication that belongs to a class of drugs called cholinesterase inhibitors. It works by blocking the breakdown of acetylcholine, a neurotransmitter in the body, leading to an increase in its levels at the neuromuscular junction. This helps to improve muscle strength and tone by enhancing the transmission of nerve impulses to muscles.

Neostigmine is primarily used in the treatment of myasthenia gravis, a neurological disorder characterized by muscle weakness and fatigue. It can also be used to reverse the effects of non-depolarizing muscle relaxants administered during surgery. Additionally, neostigmine may be used to diagnose and manage certain conditions that cause decreased gut motility or urinary retention.

It is important to note that neostigmine should be used under the close supervision of a healthcare professional due to its potential side effects, which can include nausea, vomiting, diarrhea, increased salivation, sweating, and muscle cramps. In some cases, it may also cause respiratory distress or cardiac arrhythmias.

"Indans" is not a recognized medical term or abbreviation in the field of medicine or pharmacology. It's possible that you may be referring to "indanes," which are chemical compounds that contain a indane ring structure, consisting of two benzene rings fused in an angular arrangement. Some indane derivatives have been studied for their potential medicinal properties, such as anti-inflammatory and analgesic effects. However, it's important to note that the medical use and efficacy of these compounds can vary widely and should be evaluated on a case-by-case basis under the guidance of a qualified healthcare professional.

Dibucaine is a local anesthetic drug that is used to numb the skin or mucous membranes before medical procedures. It works by blocking the nerve signals in the area where it is applied, preventing the sensation of pain. Dibucaine is available as a topical cream, ointment, or gel, and it may also be used as an ingredient in lozenges or throat sprays to relieve sore throats.

Dibucaine has been largely replaced by other local anesthetics due to its potential for causing allergic reactions and other side effects. It is important to follow your healthcare provider's instructions carefully when using dibucaine, and to inform them of any medical conditions or medications you are taking that may interact with the drug.

Tacrine is a parasympathomimetic alkaloid, which was used in the treatment of Alzheimer's disease. It works by increasing the levels of acetylcholine, a neurotransmitter in the brain that is important for memory and thinking. Tacrine was an inhibitor of acetylcholinesterase, the enzyme responsible for breaking down acetylcholine.

However, due to its significant hepatotoxicity (liver toxicity) and limited efficacy, tacrine is rarely used today. Other cholinesterase inhibitors, such as donepezil, rivastigmine, and galantamine, have largely replaced tacrine in the treatment of Alzheimer's disease.

Physostigmine is a medication that belongs to a class of drugs called cholinesterase inhibitors. It works by blocking the breakdown of a neurotransmitter called acetylcholine, which is important for communication between nerves and muscles. This results in an increase in acetylcholine levels in the body, improving nerve impulse transmission and helping to restore normal muscle function.

Physostigmine is used in the treatment of certain medical conditions that are caused by a deficiency of acetylcholine, such as myasthenia gravis, which is a neuromuscular disorder characterized by weakness and fatigue of the muscles. It may also be used to reverse the effects of certain medications that block the action of acetylcholine, such as anticholinergics, which are sometimes used in anesthesia or to treat conditions like Parkinson's disease.

It is important to note that physostigmine should only be used under the close supervision of a healthcare provider, as it can have serious side effects if not used properly.

Galantamine is a medication that belongs to a class of drugs known as cholinesterase inhibitors. It works by increasing the levels of a chemical called acetylcholine in the brain, which is important for memory and thinking skills.

Galantamine is primarily used to treat mild to moderate Alzheimer's disease, a type of dementia that affects memory, thinking, and behavior. By increasing the levels of acetylcholine, galantamine can help improve symptoms such as memory loss, confusion, and problems with speaking, writing, and understanding language.

Galantamine is available in immediate-release and extended-release tablets, as well as an oral solution. It is usually taken twice a day, typically in the morning and evening, with meals. Common side effects of galantamine include nausea, vomiting, diarrhea, and dizziness.

It's important to note that while galantamine can help improve symptoms of Alzheimer's disease, it does not cure or slow down the progression of the condition. It should only be used under the supervision of a healthcare provider.

Diazinon is a type of organophosphate insecticide that works by inhibiting the enzyme acetylcholinesterase, which leads to an accumulation of the neurotransmitter acetylcholine in the synaptic cleft and results in overstimulation of cholinergic receptors. This can cause a variety of symptoms, including muscle twitching, tremors, convulsions, and respiratory failure, which can be fatal if not treated promptly.

Diazinon is used to control a wide range of insect pests in agriculture, horticulture, and residential settings. However, it is highly toxic to both insects and mammals, including humans, and its use is regulated by environmental and public health agencies around the world. Exposure to diazinon can occur through inhalation, skin contact, or ingestion, and can cause acute and chronic health effects depending on the level and duration of exposure.

In the medical field, diazinon poisoning is treated with atropine, which blocks the action of acetylcholine at muscarinic receptors, and oximes, which reactivate acetylcholinesterase. Supportive care, such as oxygen therapy, mechanical ventilation, and fluid replacement, may also be necessary in severe cases.

Tetraisopropylpyrophosphamide (TIPP) is not typically considered a medical compound, but rather a chemical reagent used in laboratory settings for various research purposes. However, I can provide a general chemical definition for you:

Tetraisopropylpyrophosphamide (C12H28N2O4P) is an organophosphorus compound with the molecular formula [(i-Pr)2P(O)]2. It is a colorless liquid that is used as a reagent in organic synthesis, particularly for the preparation of phosphate esters and other organophosphorus compounds.

It's important to note that TIPP is highly toxic and should be handled with appropriate precautions in a laboratory setting. It can cause skin and eye irritation, respiratory problems, and may be harmful if swallowed or inhaled. Therefore, it is not used in medical treatments or therapies for patients.

Insecticides are substances or mixtures of substances intended for preventing, destroying, or mitigating any pest, including insects, arachnids, or other related pests. They can be chemical or biological agents that disrupt the growth, development, or behavior of these organisms, leading to their death or incapacitation. Insecticides are widely used in agriculture, public health, and residential settings for pest control. However, they must be used with caution due to potential risks to non-target organisms and the environment.

Parathion is not a medical term, but a chemical one. It refers to a type of organophosphate insecticide that is highly toxic and can be absorbed through the skin or ingested. Parathion works by inhibiting an enzyme called acetylcholinesterase, which leads to an overstimulation of the nervous system and can cause symptoms such as muscle twitching, convulsions, respiratory failure, and death. Although parathion is not used in medical treatments, it is important for healthcare providers to be aware of its potential health effects, particularly in cases of accidental or intentional exposure.

Organothiophosphorus compounds are a class of chemical compounds that contain carbon (organo-) and thiophosphorus bonds. Thiophosphorus refers to a phosphorus atom bonded to one or more sulfur atoms. These compounds have various applications, including use as plasticizers, flame retardants, insecticides (such as malathion and parathion), and nerve agents (such as sarin and VX). They can be synthesized through the reaction of organolithium or Grignard reagents with thiophosphoryl chloride. The general structure of these compounds is R-P(=S)Y, where R is an organic group, P is phosphorus, and Y is a group that determines the properties and reactivity of the compound.

Dichlorvos is a type of organophosphate insecticide that is used to control a wide variety of pests in agricultural, residential, and industrial settings. Its chemical formula is (2,2-dichlorovinyl) dimethyl phosphate. It works by inhibiting the enzyme acetylcholinesterase, which leads to an accumulation of the neurotransmitter acetylcholine in the synaptic clefts of nerve cells, causing overstimulation of the nervous system and ultimately death of the pest.

Dichlorvos is highly toxic to both insects and mammals, including humans. Exposure to this chemical can cause a range of symptoms, including headache, dizziness, nausea, vomiting, muscle weakness, and in severe cases, respiratory failure and death. It is classified as a Category I acute toxicant by the Environmental Protection Agency (EPA) and is listed as a hazardous substance under the Comprehensive Environmental Response, Compensation, and Liability Act (CERCLA).

Due to its high toxicity and potential for environmental persistence, dichlorvos is subject to strict regulations in many countries. It is banned or restricted for use in several jurisdictions, including the European Union, Canada, and some states in the United States. Where it is still allowed, it is typically used only under specific conditions and with appropriate safety measures in place.

Succinylcholine is a neuromuscular blocking agent, a type of muscle relaxant used in anesthesia during surgical procedures. It works by inhibiting the transmission of nerve impulses at the neuromuscular junction, leading to temporary paralysis of skeletal muscles. This facilitates endotracheal intubation and mechanical ventilation during surgery. Succinylcholine has a rapid onset of action and is metabolized quickly, making it useful for short surgical procedures. However, its use may be associated with certain adverse effects, such as increased heart rate, muscle fasciculations, and potentially life-threatening hyperkalemia in susceptible individuals.

Pyridostigmine Bromide is a medication that belongs to the class of drugs known as cholinesterase inhibitors. It is primarily used in the treatment of myasthenia gravis, a neuromuscular disorder characterized by muscle weakness and fatigue.

Pyridostigmine works by blocking the action of acetylcholinesterase, an enzyme that breaks down acetylcholine, a neurotransmitter essential for muscle contraction. By preventing the breakdown of acetylcholine, pyridostigmine helps to increase its levels at the neuromuscular junction, thereby improving muscle strength and function.

The bromide salt form of pyridostigmine is commonly used because it is more soluble in water, which makes it easier to administer orally as a liquid or tablet. The medication's effects typically last for several hours, and its dosage may be adjusted based on the patient's response and any side effects experienced.

Common side effects of pyridostigmine include nausea, vomiting, diarrhea, increased salivation, sweating, and muscle cramps. In some cases, higher doses of the medication can lead to more severe side effects such as respiratory distress, seizures, or cardiac arrhythmias. Therefore, it is essential to monitor patients closely while they are taking pyridostigmine and adjust the dosage as necessary to minimize side effects and optimize treatment outcomes.

Fenitrothion is a type of organophosphate pesticide that is used to control a wide variety of insects. It works by inhibiting the enzyme acetylcholinesterase, which leads to an accumulation of the neurotransmitter acetylcholine and results in nervous system dysfunction in insects.

Fenitrothion is used to control pests in agricultural settings, as well as in public health programs to combat vectors of diseases such as mosquitoes and lice. However, it can also have toxic effects on non-target organisms, including humans, and has been linked to a variety of health problems, including neurological damage and cancer. As a result, its use is regulated in many countries, and there are restrictions on the amount that can be applied and the circumstances under which it can be used.

Carbaryl is a carbamate pesticide that is used to control a wide variety of insects, including fleas, ticks, and mosquitoes. It works by inhibiting the action of an enzyme called cholinesterase, which is necessary for the proper functioning of the nervous system in insects. This leads to paralysis and death of the pests. Carbaryl is also used in some veterinary products to treat parasitic infestations. It can be found in various forms, such as powders, granules, and solutions, and can be applied to plants, animals, and indoor/outdoor surfaces. However, it can be harmful to non-target organisms, including humans, if not used properly. Therefore, it is important to follow the label instructions carefully when using carbaryl products.

Methomyl is a carbamate insecticide that acts as a reversible inhibitor of acetylcholinesterase, an enzyme that breaks down the neurotransmitter acetylcholine in nerve synapses. This results in an accumulation of acetylcholine, leading to overstimulation of cholinergic receptors and disruption of normal nervous system function. Methomyl is used to control a wide range of pests in various crops, but its use is restricted due to its high toxicity to non-target organisms, including humans. It can be absorbed through the skin, respiratory tract, or gastrointestinal tract and can cause symptoms such as nausea, vomiting, diarrhea, muscle twitching, weakness, and difficulty breathing in cases of acute exposure. Chronic exposure to methomyl has been linked to neurological effects, including memory loss and decreased cognitive function.

Carbamates are a group of organic compounds that contain the carbamate functional group, which is a carbon atom double-bonded to oxygen and single-bonded to a nitrogen atom (> N-C=O). In the context of pharmaceuticals and agriculture, carbamates are a class of drugs and pesticides that have carbamate as their core structure.

Carbamate insecticides work by inhibiting the enzyme acetylcholinesterase, which is responsible for breaking down the neurotransmitter acetylcholine in the synapses of the nervous system. When this enzyme is inhibited, acetylcholine accumulates in the synaptic cleft, leading to overstimulation of the nervous system and ultimately causing paralysis and death in insects.

Carbamate drugs are used for a variety of medical indications, including as anticonvulsants, muscle relaxants, and psychotropic medications. They work by modulating various neurotransmitter systems in the brain, such as GABA, glutamate, and dopamine. Carbamates can also be used as anti- parasitic agents, such as ivermectin, which is effective against a range of parasites including nematodes, arthropods, and some protozoa.

It's important to note that carbamate pesticides can be toxic to non-target organisms, including humans, if not used properly. Therefore, it's essential to follow all safety guidelines when handling or using these products.

Butyrylthiocholine is a synthetic chemical compound that is often used in scientific research, particularly in the study of enzymes and neurotransmitters. It is the substrate for the enzyme butyrylcholinesterase, which is found in the blood and helps to break down certain types of drugs and neurotransmitters.

In biochemical terms, butyrylthiocholine is a choline ester of butyric acid, with a thio (sulfur) group replacing one of the oxygen atoms in the ester linkage. This structural feature makes it an excellent substrate for butyrylcholinesterase, as the sulfur atom can form a covalent bond with the enzyme's active site, leading to rapid and specific catalysis.

It is important to note that butyrylthiocholine itself does not have any direct medical relevance, but rather serves as a tool for studying the mechanisms of enzymes and other biological processes.

Soman is a chemical compound with the formula (CH3)2(C=O)N(CH2)4SH. It is a potent nerve agent, a type of organic compound that can cause death by interfering with the nervous system's ability to regulate muscle movement. Soman is an odorless, colorless liquid that evaporates slowly at room temperature and is therefore classified as a "v-type" or "volatile" nerve agent. It is considered to be one of the most toxic substances known. Exposure to soman can occur through inhalation, skin contact, or ingestion, and it can cause a range of symptoms including nausea, seizures, respiratory failure, and death.

A Mass Casualty Incident (MCI) is a situation in which the number of injured or deceased individuals exceeds the local resources available to respond and manage the incident. It typically involves multiple victims, often resulting from natural disasters, transportation accidents, terrorist attacks, or industrial incidents. The severity and scale of injuries require additional resources, coordination, and response from regional, national, or international emergency management and healthcare systems.

Cholinesterase reactivators are drugs that reverse the inhibition of cholinesterase by organophosphates or sulfonates. They are ... v t e v t e (Cholinesterase reactivators, All stub articles, Pharmacology stubs, Toxicology stubs). ... Acetylcholinesterase inhibitor Nerve agent "Cholinesterase Reactivators - MeSH - NCBI". www.ncbi.nlm.nih.gov. Antonijevic, B.; ...
2015 Jokanović M, Prostran M (2009). "Pyridinium oximes as cholinesterase reactivators. Structure-activity relationship and ... Significant advances with cholinesterases (ChEs), specifically human serum BChE (HuBChE) have been made. HuBChe can offer a ... "Cholinesterase Inhibition". Archived from the original on 2013-04-02. "Pesticide Application and Safety Training for ... He was later transferred to Berlin, where poisoning by a cholinesterase inhibitor was diagnosed and confirmed by multiple tests ...
Jokanović M, Prostran M (2009). "Pyridinium oximes as cholinesterase reactivators. Structure-activity relationship and efficacy ... "Current understanding of the application of pyridinium oximes as cholinesterase reactivators in treatment of organophosphate ... Cholinesterase reactivators, Aldoximes, Peripherally selective drugs, Quaternary ammonium compounds). ...
Jokanović M, Prostran M (2009). "Pyridinium oximes as cholinesterase reactivators. Structure-activity relationship and efficacy ... Cholinesterase reactivators, Chemical substances for emergency medicine, Ethers, Aldoximes, Quaternary ammonium compounds). ...
Petroianu, Georg (2015). "History of organophosphorus cholinesterase inhibitors & reactivators". Military Medical Science ... Historical development of organophosphorus cholinesterase inhibitors"". Cholinesterases and Anticholinesterase Agents. Handbook ... doi:10.1007/978-3-642-68441-8. ISBN 978-3-642-68443-2. S2CID 33095322.The history of cholinesterase inhibitors: who was ... TEPP was discovered to be an inhibitor of cholinesterases. Schrader referred to the studies by Eberhard Gross, who was the ...
Cholinesterase Reactivators, Psychochemicals and Irritants and Vesicants. Vol. 2. Commission on Life Sciences. The National ...
V. The effect of oximes and related cholinesterase reactivators". Teratology. 15 (1): 33-42. doi:10.1002/tera.1420150105. PMID ...
Similarly, cholinesterase reactivators antidotes such as 2-PAM were tested on about 750 subjects. These agents are still used ... 2, "Cholinesterase Reactivators, Psychochemicals and Irritants and Vesicants" (1984) Vol. 3, "Final Report: Current Health ... 2, "Cholinesterase Reactivators, Psychochemicals and Irritants and Vesicants (1984) Vol. 3, "Final Report: Current Health ... 2, "Cholinesterase Reactivators, Psychochemicals and Irritants and Vesicants (1984) Vol. 3, "Final Report: Current Health ...
Administration of a cholinesterase reactivator, in the pyridinium oxime family, usually pralidoxime; Administration of ... However, cholinesterase inhibition is caused by all anticholinesterase compounds and is therefore not a specific biomarker for ... Two pools of cholinesterases exist in the blood: acetylcholinesterase in erythrocytes and pseudocholinesterase in plasma. The ... In addition, the activity of cholinesterases in the blood varies in populations and there are no studies which have measured a ...
However, since the inhibited enzyme ages so rapidly, the inhibited enzyme can't be reactivated by cholinesterase reactivators. ... "The summary on non-reactivation cholinergic properties of oxime reactivators: the interaction with muscarinic and nicotinic ...
... meaning the acetylcholinesterase inhibited by MFPCh can't be reactivated by cholinesterase reactivators. MFPCh also acts ... "Experiments with Methyl-fluoro-phosphorylcholine-inhibited Cholinesterase". Acta Chemica Scandinavica. 12: 780-781. doi:10.3891 ...
... reacts with the acetylcholinesterase to form an aged enzyme adduct that can't be reactivated by cholinesterase reactivators. EA ... Guanitoxin Chabrier, P. E.; Jacob, J. (May 1980). "In vivo and in vitro inhibition of cholinesterase by methyl-1 (S methyl ...
... insecticide that is an irreversible acetylcholinesterase inhibitor and is resistant to cholinesterase reactivators. It was ...
Possible Long-Term Health Effects of Short-Term Exposure To Chemical Agents, Volume 2: Cholinesterase Reactivators, ...
Cholinesterase Reactivators, Psychochemicals and Irritants and Vesicants. The National Academies Press. p. 79. ISBN 978-0-309- ...
... enzyme reactivators MeSH D27.505.519.405.347 - cholinesterase reactivators MeSH D27.505.519.421 - fibrin modulating agents MeSH ... cholinesterase inhibitors MeSH D27.505.519.625.120.400 - cholinesterase reactivators MeSH D27.505.519.625.150 - dopamine agents ... cholinesterase inhibitors MeSH D27.505.696.577.120.400 - cholinesterase reactivators MeSH D27.505.696.577.150 - dopamine agents ... cholinesterase inhibitors MeSH D27.505.519.389.310 - cyclooxygenase inhibitors MeSH D27.505.519.389.310.500 - cyclooxygenase 2 ...
Cholinesterase reactivators, Aldoximes, Carboxamides, Pyridinium compounds, Chlorides, All stub articles, Pharmacology stubs). ...
Cholinesterase reactivators, Chemical substances for emergency medicine, Aldoximes, Pyridinium compounds, All stub articles, ...
... can also bind to other esterases, e.g., AChE, cholinesterase (ChE) and carboxylesterases (CarbE). In this binding, soman ... oxime reactivators. The rate of this process is dependent on the OP. Soman is an OP that stimulates the rate of aging most ... interfering with normal functioning of the mammalian nervous system by inhibiting the enzyme cholinesterase. It is an inhibitor ... "Behavioral Changes in the Rat after Low Doses of Cholinesterase Inhibitors". Toxicological Sciences. 4 (2part2): 195-208. doi: ...
McHardy SF, Wang HL, McCowen SV, Valdez MC (April 2017). "Recent advances in acetylcholinesterase Inhibitors and Reactivators: ... a reversible cholinesterase inhibitor. It occurs naturally in the Calabar bean and the fruit of the Manchineel tree. The ...
Cholinesterase reactivators are drugs that reverse the inhibition of cholinesterase by organophosphates or sulfonates. They are ... v t e v t e (Cholinesterase reactivators, All stub articles, Pharmacology stubs, Toxicology stubs). ... Acetylcholinesterase inhibitor Nerve agent "Cholinesterase Reactivators - MeSH - NCBI". www.ncbi.nlm.nih.gov. Antonijevic, B.; ...
The goal of study was the determination of the ionization constants for the oximes - cholinesterases reactivators in aqueous ... Spectrophotometric Determination of the Ionization Constants for the Oximes - Cholinesterases Reactivators at Different ... and the ionization constants for the oxime cholinesterases reactivators (isonitrosin, pralidoxime, dipyroxime, toxogonin, ... A hypothesis that the temperature affects the oximes ability to reactivate phosphorylated cholinesterases has been proposed. ...
Cholinesterase reactivators: oxime compounds are used, eg. Diacetyl monoxime, pralidoxime chloride, pralidoxime iodide, ... They are irreversible competitive inhibitors of enzyme Acetyl Cholinesterase. Site of action is myo-neural junction snd ...
Literature Cited in Cholinesterase Inhibitors: Including Insecticides and Chemical Warfare Nerve Agents ... Xue SZ, Ding XJ, Ding Y. Clinical observation and comparison of the effectiveness of several oxime cholinesterase reactivators ... Namba T. Cholinesterase inhibition by organophosphorus compounds and its clinical effects. Bulletin of the World Health ... Karalliedde L. Cholinesterase estimations revisited: the clinical relevance. European Journal of Anaesthesiology. May 2002;19(5 ...
Kuca K, Jun D, Bajgar J. Currently used cholinesterase reactivators against nerve agent intoxication: comparison of their ... The reactivatibility of cholinesterase inhibited by VX and sarin in man. Toxicol Appl Pharmacol. 1974 Feb. 27(2):241-52. [QxMD ... Reactivation of VX-inhibited cholinesterase by 2-PAM and HS-6 in rats. Drug Chem Toxicol. 1983. 6(3):235-40. [QxMD MEDLINE Link ... Bajgar J, Kuca K, Fusek J, Karasova J, Kassa J, Cabal J. Inhibition of blood cholinesterases following intoxication with VX and ...
... with reactivators of cholinesterase are effective antidotal agents for the acute toxic effects of fensulfothion. Short-term ... RBC cholinesterase inhibition was observed at 2 ppm while plasma and brain levels were unaffected. No cholinesterase depression ... cholinesterase activity in females is more sensitive to in vivo anti-cholinesterase activity. This is possibly a result of a ... Inhibition of cholinesterase was observed in serum and RBC at 2 ppm and above. At 5 ppm and 10 ppm signs of cholinergic ...
Pralidoxime, a cholinesterase reactivator, is important for patients with organophosphorus poisoning, but its usefulness in ... Although a plasma cholinesterase level was not detectable on admission, the patients red blood cell cholinesterase level was ... Convalescent cholinesterase levels could not be obtained. Case 2. On May 12, 1997, a 2-year-old girl was observed by her ...
Pyridinium oximes with ortho-positioned halogen moiety are effective reactivators of cholinesterases inhibited by nerve agents ...
Cholinesterase Reactivators MeSH DeCS ID:. 938 Unique ID:. D000931 Documents indexed in the Virtual Health Library (VHL):. ...
Cholinesterase reactivator: Pralidoxime chloride.. *Cholinergic Blocking agents: SAR of cholinolytic agents. Solanaceous ... Indirect acting/ Cholinesterase inhibitors (Reversible & Irreversible):. *Physostigmine, Neostigmine*, Pyridostigmine, ...
Members of this group are CHOLINESTERASE REACTIVATORS. Descriptor ID. D010091 MeSH Number(s). D02.092.570.665 ...
The organophosphorus inhibited activity is regained in the presence of cholinesterase reactivator. Moreover, the enzyme ... Direct visualization of cholinesterase activity on polyacrylamide gels is routinely practiced using acetylthiocholine as a ... Secondly, the hemolysate cholinesterase activity, as well as its inhibition by organophosphorus pesticides is understandable ... Our results prove that 1-NA is an alternative substrate of hemolysate cholinesterase which specifically detects the enzyme ...
However, pyridostigmine and cholinesterase reactivators currently used in the armed forces do not protect/reactivate central ... Organophosphates (OPs) inhibit the enzyme cholinesterase and cause accumulation of acetylcholine, and are known to cause ... an AChE reactivator (oxime), and an anticonvulsant, such as diazepam. The inclusion of diazepam (Valium) in the treatment ... Many Western countries pre-treat military populations with the reversible cholinesterase inhibitor pyridostigmine bromide to ...
... an oxime type cholinesterase reactivator by HPLC with electrochemical detection from different biological samples., J. ... a novel oxime-type cholinesterase reactivator, Journal of Chromatography, A., 1122, 84-87, 2006. ...
Cholinesterase Inhibitors:chemistry, Cholinesterase Reactivators:chemistry, Enzymes, Immobilized:antagonists & inhibitors, ... CONCLUSION: Our work gives comparison of efficacy of reactivators in dependence on the length of alkylene chain and position of ... Evaluation of effectivity of aldoxime reactivators is provided by simple means. The method allows rapid in vitro evaluation of ... the reactivators without being disturbed by excess of the organophosphate or reactivator.... ...
... were evaluated as reversible inhibitors of cholinesterase and/or reactivators of enzymes inhibited by toxic organophosphorus ... "RB-reactivator screening" as a novel cell-based assay for discoveries of molecular targeting agents including the first-in- ... Potential of Vitamin B6 Dioxime Analogues to Act as Cholinesterase Ligands. Gaso Sokac, Dajana; Zandona, Antonio; Roca, Suncica ... I termed this screening as "RB-reactivator screening". Using the screening systems for agents that up-regulate the expression ...
Cholinesterase Reactivators, Psychochemicals, and Irritants and Vesicants 1984 of the Kingdom of Koryo, when opinion was ...
... a cholinesterase reactivator, prallidoxime (4 pg per 500 ml blood), was introduced to reactivate the cholinesterase in the two ... Cholinesterase activity was assessed in two blood samples by measuring the changes in absorbence at 405 nm (EPOS 5060 analyser ... To ensure that high ambient temperatures had not reduced the cholinesterase activity, a standard solution of pure enzyme was ... In control samples a large concentration of 2-hydmxyethylbenzthiazol (200 mg/ml) had no detectable effect on cholinesterase ...
Methomyl poisoning treatment disables oxime reactivators; this prevents reactivation of cholinesterase, and thus hinders the ... Once methomyl enters the body, it forms a complex with acetyl cholinesterase. Acetyl cholinesterase activity is depended ton a ... The cholinesterase levels of patients 3, 4, and 5were low, but they did not have obvious symptoms of methomyl poisoning. ... A. The activity assay result for cholinesterase was 1125.40 U/L (normal: 4000-13000U/L) and AST was 9 U/L (normal:15-40 U/L); ...
cholinesterase reactivators. *chondroitin. *chondroitin polysulfate. *Chooz. *Chrysanthemum parethenium. *Cialis. *Cibinqo. * ...
OP pesticides inhibit carboxylic esterase enzymes including acetyl cholinesterase (AChE) and plasma cholinesterase (PChE) ... It was observed that in spite of clear reactivation of acetyl cholinesterase no clinical benefit could be achieved (19). They ... The other agent that has been used for four decades is pralidoxime, which acts by reactivating phosphorylated cholinesterase (1 ... Prasad DRMM, Jirli PS, Mahesh M, Mamatha S. Relevance of Plasma Cholinesterase to Clinical Findings in Acute Organophosphorous ...
Organophosphate Insecticide Antagonists use Cholinesterase Reactivators Organophosphate Insecticides use Insecticides, ... Organothiophosphate Insecticide Antagonists use Cholinesterase Reactivators Organothiophosphate Insecticides use Insecticides, ...
Organophosphate Insecticide Antagonists use Cholinesterase Reactivators Organophosphate Insecticides use Insecticides, ... Organothiophosphate Insecticide Antagonists use Cholinesterase Reactivators Organothiophosphate Insecticides use Insecticides, ...
Organophosphate Insecticide Antagonists use Cholinesterase Reactivators Organophosphate Insecticides use Insecticides, ... Organothiophosphate Insecticide Antagonists use Cholinesterase Reactivators Organothiophosphate Insecticides use Insecticides, ...
Organophosphate Insecticide Antagonists use Cholinesterase Reactivators Organophosphate Insecticides use Insecticides, ... Organothiophosphate Insecticide Antagonists use Cholinesterase Reactivators Organothiophosphate Insecticides use Insecticides, ...
Organophosphate Insecticide Antagonists use Cholinesterase Reactivators Organophosphate Insecticides use Insecticides, ... Organothiophosphate Insecticide Antagonists use Cholinesterase Reactivators Organothiophosphate Insecticides use Insecticides, ...
Organophosphate Insecticide Antagonists use Cholinesterase Reactivators Organophosphate Insecticides use Insecticides, ... Organothiophosphate Insecticide Antagonists use Cholinesterase Reactivators Organothiophosphate Insecticides use Insecticides, ...
Organophosphate Insecticide Antagonists use Cholinesterase Reactivators Organophosphate Insecticides use Insecticides, ... Organothiophosphate Insecticide Antagonists use Cholinesterase Reactivators Organothiophosphate Insecticides use Insecticides, ...
Organophosphate Insecticide Antagonists use Cholinesterase Reactivators Organophosphate Insecticides use Insecticides, ... Organothiophosphate Insecticide Antagonists use Cholinesterase Reactivators Organothiophosphate Insecticides use Insecticides, ...
Organophosphate Insecticide Antagonists use Cholinesterase Reactivators Organophosphate Insecticides use Insecticides, ... Organothiophosphate Insecticide Antagonists use Cholinesterase Reactivators Organothiophosphate Insecticides use Insecticides, ...
  • Although a plasma cholinesterase level was not detectable on admission, the patient's red blood cell cholinesterase level was normal when measured after completion of pralidoxime therapy. (cdc.gov)
  • The other agent that has been used for four decades is pralidoxime, which acts by reactivating phosphorylated cholinesterase (1). (ac.ir)
  • Cholinesterase reactivators are drugs that reverse the inhibition of cholinesterase by organophosphates or sulfonates. (wikipedia.org)
  • Following intraperitoneal administration of fensulfothion (0.9 mg/kg) to rats, inhibition of cholinesterase was maximal within one hour. (inchem.org)
  • OP pesticides inhibit carboxylic esterase enzymes including acetyl cholinesterase (AChE) and plasma cholinesterase (PChE) through binding to the esteratic site on the AChE molecule, phosphorylating the enzyme. (ac.ir)
  • Bovine erythrocyte acetylcholinesterase and human plasma cholinesterase are irreversibly inhibited by diethylmesoxalate hydrate, the inhibition potency being comparable to that of certian insecticidal organophosphates and carbamates. (inra.fr)
  • They are irreversible competitive inhibitors of enzyme Acetyl Cholinesterase. (pediatriconcall.com)
  • Prallidoxime will also remove organophosphates attached to the activity site of the cholinesterase causing an increase in enzyme activity. (dlawer.info)
  • Organophosphate Poisoning and Carbamate Poisoning Organophosphates and carbamates are common insecticide ingredients that inhibit cholinesterase activity, causing acute muscarinic manifestations (eg, salivation, lacrimation, urination, diarrhea. (msdmanuals.com)
  • Spectrophotometric and electrochemical study of protolytic equilibria of some oximes-acetylcholinesterase reactivators. (bmc-rm.org)
  • Moreover, the enzyme activity bands formed using 1-NA proves the specificity of the substrate for hemolysate cholinesterase as in the presence of specific acetylcholinesterase inhibitors the band formation disappears. (who.int)
  • The designation "nerve gas" or "nerve agent" is used for organophosphorus compounds that inhibit tissue cholinesterase. (who.int)
  • A hypothesis that the temperature affects the oximes ability to reactivate phosphorylated cholinesterases has been proposed. (bmc-rm.org)
  • To exclude genetic or nutritional causes for the low enzyme activity, a cholinesterase reactivator, prallidoxime (4 pg per 500 ml blood), was introduced to reactivate the cholinesterase in the two samples and in the controls. (dlawer.info)
  • As with several other compounds of a similar structural nature, cholinesterase activity in females is more sensitive to in vivo anti-cholinesterase activity. (inchem.org)
  • In control samples a large concentration of 2 - hydmxyethylbenzthiazol (200 mg/ml) had no detectable effect on cholinesterase activity either immediately or after five days' incubation at room temperature. (dlawer.info)
  • Our results prove that 1-NA is an alternative substrate of hemolysate cholinesterase which specifically detects the enzyme activity on gel rapidly. (who.int)
  • The goal of study was the determination of the ionization constants for the oximes - cholinesterases reactivators in aqueous solutions at different temperatures. (bmc-rm.org)
  • To ensure that high ambient temperatures had not reduced the cholinesterase activity, a standard solution of pure enzyme was kept at 25oC for five days. (dlawer.info)
  • Hemolysate cholinesterase is currently recognized as the most preferred biomarker to detect acute organophosphorus poisoning. (who.int)
  • Secondly, the hemolysate cholinesterase activity, as well as its inhibition by organophosphorus pesticides is understandable within 10 min using Fast Blue RR dye for the detection of 1-NA. (who.int)
  • The organophosphorus inhibited activity is regained in the presence of cholinesterase reactivator. (who.int)
  • Direct visualization of cholinesterase activity on polyacrylamide gels is routinely practiced using acetylthiocholine as a substrate. (who.int)
  • Here, we have explored alternative substrates, such as 1-NA and 2-NA which might have the potential to behave as specific substrates for the detection of hemolysate cholinesterase activity on the gels. (who.int)
  • We recommend 1-NA for rapid detection of hemolysate cholinesterase activity on the gels. (who.int)
  • Cholinesterase activity was assessed in two blood samples by measuring the changes in absorbence at 405 nm (EPOS 5060 analyser) resulting when the chromogen 5,5'?dithiobis(4-nitrobenzoic acid) reacts with the thiocholine iodide produced by the action of the enzyme on a highly diluted sample of acetylthiocholine iodide. (dlawer.info)
  • There was only a very small and not significant decrease in cholinesterase activity. (dlawer.info)
  • Therefore, the need arises to explore rapid detection methods, which can specifically detect hemolysate cholinesterase on polyacrylamide gels. (who.int)
  • Convalescent cholinesterase levels could not be obtained. (cdc.gov)
  • The cholinesterase levels of patients 3, 4, and 5were low, but they did not have obvious symptoms of methomyl poisoning. (biomedres.us)
  • One of the main problems in the treatment of poisoning with organophosphorus (OPs) inhibitors of acetylcholinesterase (AChE) is low ability of existing reactivators of AChE that are used as antidotes to cross the blood-brain barrier (BBB). (inra.fr)
  • In vitro effects of acetylcholinesterase inhibitors and reactivators on Complex I of electron transport chain. (nel.edu)
  • Cholinesterase Inhibitors" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus, MeSH (Medical Subject Headings) . (umassmed.edu)
  • This graph shows the total number of publications written about "Cholinesterase Inhibitors" by people in this website by year, and whether "Cholinesterase Inhibitors" was a major or minor topic of these publications. (umassmed.edu)
  • Below are the most recent publications written about "Cholinesterase Inhibitors" by people in Profiles. (umassmed.edu)
  • Cholinesterase reactivators are drugs that reverse the inhibition of cholinesterase by organophosphates or sulfonates. (wikipedia.org)
  • After aging has occurred, common therapeutics like oximes cannot reactivate the cholinesterase enzyme and relieve cholinergic inhibition. (cdc.gov)
  • The efficacy of oxime reactivators was subsequently tested in a kinetics study by Davies and colleagues who then reported a two-stage chemical process of ChE inhibition by organophosphorus compounds (OPs). (cdc.gov)
  • Drugs that inhibit cholinesterases. (lookformedical.com)
  • The compounds inhibit cholinesterases and amyloid beta (Abeta) fibrillation, protect against Abeta42-induced toxicity in vitro, and demonstrate efficacy in vivo in a transgenic Caenorhabditis elegans model expressing Abeta42, with potencies similar to rivastigmine and natural polyphenols. (inrae.fr)
  • Cholinergic muscarinic antagonist + cholinesterase reactivator. (empr.com)
  • When cholinesterases are inhibited, the action of endogenously released acetylcholine at cholinergic synapses is potentiated. (lookformedical.com)
  • Standard therapy of NA poisoning generally involves administration of anticholinergic atropine and an oxime reactivator of phosphylated AChE. (nih.gov)
  • In this work, modified cationic liposomes were developed that can penetrate through the BBB and deliver the reactivator of AChE pralidoxime chloride (2-PAM) into the brain. (inra.fr)
  • A promising reactivator based on tetrahydroacridine linked to a nonquaternary oxime is also an undesired submicromolar reversible inhibitor of AChE. (inrae.fr)
  • Pralidoxime chloride is a cholinesterase reactivator. (nih.gov)
  • We thus show that rational design based on structural studies permits the refinement of new-generation pyridine aldoxime reactivators that may be more effective in the treatment of nerve agent intoxication. (inrae.fr)
  • An agent used as a substrate in assays for cholinesterases, especially to discriminate among enzyme types. (lookformedical.com)
  • Action of diethixime, a new cholinesterase reactivator, on the central nervous system. (cdc.gov)
  • Predictors of Cholinesterase Discontinuation during the First Year after Nursing Home Admission. (umassmed.edu)