Acetylcholinesterase
Cholinesterase Inhibitors
Acetylthiocholine
Cholinesterases
Cholinesterase Reactivators
Electrophorus
Tacrine
Physostigmine
Torpedo
Galantamine
Pralidoxime Compounds
Sarin
Isoflurophate
Thiocholine
Edrophonium
Electric Organ
Organothiophosphorus Compounds
Chlorpyrifos
Insecticides
Pyridostigmine Bromide
Soman
Bungarus
Neostigmine
Carbamates
Phenylcarbamates
Organophosphates
Echothiophate Iodide
Tetraisopropylpyrophosphamide
Elapid Venoms
Oximes
Organophosphate Poisoning
Malathion
Organophosphorus Compounds
Chemical Warfare Agents
Obidoxime Chloride
Butyrylthiocholine
Choline O-Acetyltransferase
Acetylcholine
Trichlorfon
Histocytochemistry
Organothiophosphates
Parathion
Motor Endplate
Brain
Receptors, Cholinergic
Benzyl Compounds
Pyridinium Compounds
Pesticides
Binding Sites
Erythrocytes
Nootropic Agents
Dimethoate
Decamethonium Compounds
Alzheimer Disease
Propidium
Why are there so few resistance-associated mutations in insecticide target genes? (1/2082)
The genes encoding the three major targets of conventional insecticides are: Rdl, which encodes a gamma-aminobutyric acid receptor subunit (RDL); para, which encodes a voltage-gated sodium channel (PARA); and Ace, which encodes insect acetylcholinesterase (AChE). Interestingly, despite the complexity of the encoded receptors or enzymes, very few amino acid residues are replaced in different resistant insects: one within RDL, two within PARA and three or more within AChE. Here we examine the possible reasons underlying this extreme conservation by looking at the aspects of receptor and/or enzyme function that may constrain replacements to such a limited number of residues. (+info)Calcitonin gene-related peptide decreases expression of acetylcholinesterase in mammalian myotubes. (2/2082)
Nerve-derived trophic factors are known to modulate expression of acetylcholinesterase (AChE) in skeletal muscle fibers, yet the precise identity of these factors remains elusive. In the present study, we treated mouse C2 myotubes with calcitonin gene-related peptide (CGRP). Compared to non-treated myotubes, cell-associated AChE activity levels were decreased by approximately 60% after 48 h of treatment. A parallel reduction in AChE total protein levels was also observed as determined by Western blot analysis. The reduction in AChE activity was due to a decrease in the levels of the G1 molecular form and to an elimination of G1. By contrast, levels of secreted AChE remained unchanged following CGRP treatment. Finally, the overall decrease in AChE activity was accompanied by a reduction in AChE transcripts which could not be attributed to changes in the transcriptional rate of the ACHE gene. (+info)Monoclonal antibody 3F3 against conformational epitope of Torpedo acetylcholinesterase. (3/2082)
AIM: To study the type of epitope of native Torpedo acetylcholinesterase (AChE) directed by its monoclonal antibody (McAb) 3F3. METHODS: Enzyme-linked immunosorbent assay (ELISA) was used for the assay of the reaction between antigen and antibody. RESULTS: McAb 3F3 immunoreacted well with the native AChE, but not with the reduced- and alkylated-AChE (RA-AChE) at all. Soman did not interfere the binding of 3F3 with AChE molecule. The synthesized 24-peptide containing the active serine residue of the AChE active center did not react with McAb 3F3. CONCLUSION: 3F3 is a monoclonal antibody against the conformational epitope of Torpedo AChE active center, but dose not occupy the active serine residue of the enzyme. (+info)Establishment and characterization of human neuroblastoma cell lines. (4/2082)
Three new tissue culture cell lines, CHP-100, CHP-126, and CHP-134, have been established from explant cultures of human neuroblastoma. The cell lines have been characterized with respect to morphology, chromosomes constitution, growth, neural enzyme content, and their ability to grow in nude mice. The cells grow as dense masses comprised of fibroblast-or neuroblast-like cells with small processes. The cell lines differ in their neural enzyme acitivity. The chromosomal content of the 3 cell lines is near diploid, and all are capable of forming tumors in nude mice. The morphological findings indicate that the cells in culture resemble those found in the tumor, and the enzyme activities are consistent with those of nervous tissue. This the morphological, biochemical, and tumorigenic properties confirm that the 3 cell lines are neoplastic cells of neural origin. (+info)Electron paramagnetic resonance reveals altered topography of the active center gorge of acetylcholinesterase after binding of fasciculin to the peripheral site. (5/2082)
Fasciculin, a peptidic toxin from snake venom, inhibits mammalian and fish acetylcholinesterases (AChE) by binding to the peripheral site of the enzyme. This site is located at the rim of a narrow, deep gorge which leads to the active center triad, located at its base. The proposed mechanisms for AChE inhibition by fasciculin include allosteric events resulting in altered conformation of the AChE active center gorge. However, a fasciculin-induced altered topography of the active center gorge has not been directly demonstrated. Using electron paramagnetic resonance with the spin-labeled organophosphate 1-oxyl-2,2,6, 6-tetramethyl-4-piperidinylethylphosphorofluoridate (EtOSL) specifically bound to the catalytic serine of mouse AChE (mAChE), we show that bound fasciculin on mAChE slows down, but does not prevent phosphorylation of the active site serine by EtOSL and protects the gorge conformation against thermal denaturation. Most importantly, a restricted freedom of motion of the spin label bound to the fasciculin-associated mAChE, compared to mAChE, is evidenced. Molecular models of mAChE and fasciculin-associated mAChE with tethered EtOSL enantiomers indicate that this restricted motion is due to greater proximity of the S-EtOSL nitroxide radical to the W86 residue in the fasciculin-associated enzyme. Our results demonstrate a topographical alteration indicative of a restricted conformation of the active center gorge of mAChE with bound fasciculin at its rim. (+info)Organophosphorylation of acetylcholinesterase in the presence of peripheral site ligands. Distinct effects of propidium and fasciculin. (6/2082)
Structural analysis of acetylcholinesterase (AChE) has revealed two sites of ligand interaction in the active site gorge: an acylation site at the base of the gorge and a peripheral site at its mouth. A goal of our studies is to understand how ligand binding to the peripheral site alters the reactivity of substrates and organophosphates at the acylation site. Kinetic rate constants were determined for the phosphorylation of AChE by two fluorogenic organophosphates, 7-[(diethoxyphosphoryl)oxy]-1-methylquinolinium iodide (DEPQ) and 7-[(methylethoxyphosphonyl)oxy]-4-methylcoumarin (EMPC), by monitoring release of the fluorescent leaving group. Rate constants obtained with human erythrocyte AChE were in good agreement with those obtained for recombinant human AChE produced from a high level Drosophila S2 cell expression system. First-order rate constants kOP were 1,600 +/- 300 min-1 for DEPQ and 150 +/- 11 min-1 for EMPC, and second-order rate constants kOP/KOP were 193 +/- 13 microM-1 min-1 for DEPQ and 0.7-1.0 +/- 0.1 microM-1 min-1 for EMPC. Binding of the small ligand propidium to the AChE peripheral site decreased kOP/KOP by factors of 2-20 for these organophosphates. Such modest inhibitory effects are consistent with our recently proposed steric blockade model (Szegletes, T., Mallender, W. D., and Rosenberry, T. L. (1998) Biochemistry 37, 4206-4216). Moreover, the binding of propidium resulted in a clear increase in kOP for EMPC, suggesting that molecular or electronic strain caused by the proximity of propidium to EMPC in the ternary complex may promote phosphorylation. In contrast, the binding of the polypeptide neurotoxin fasciculin to the peripheral site of AChE dramatically decreased phosphorylation rate constants. Values of kOP/KOP were decreased by factors of 10(3) to 10(5), and kOP was decreased by factors of 300-4,000. Such pronounced inhibition suggested a conformational change in the acylation site induced by fasciculin binding. As a note of caution to other investigators, measurements of phosphorylation of the fasciculin-AChE complex by AChE inactivation gave misleading rate constants because a small fraction of the AChE was resistant to inhibition by fasciculin. (+info)Genetic analysis of collagen Q: roles in acetylcholinesterase and butyrylcholinesterase assembly and in synaptic structure and function. (7/2082)
Acetylcholinesterase (AChE) occurs in both asymmetric forms, covalently associated with a collagenous subunit called Q (ColQ), and globular forms that may be either soluble or membrane associated. At the skeletal neuromuscular junction, asymmetric AChE is anchored to the basal lamina of the synaptic cleft, where it hydrolyzes acetylcholine to terminate synaptic transmission. AChE has also been hypothesized to play developmental roles in the nervous system, and ColQ is also expressed in some AChE-poor tissues. To seek roles of ColQ and AChE at synapses and elsewhere, we generated ColQ-deficient mutant mice. ColQ-/- mice completely lacked asymmetric AChE in skeletal and cardiac muscles and brain; they also lacked asymmetric forms of the AChE homologue, butyrylcholinesterase. Thus, products of the ColQ gene are required for assembly of all detectable asymmetric AChE and butyrylcholinesterase. Surprisingly, globular AChE tetramers were also absent from neonatal ColQ-/- muscles, suggesting a role for the ColQ gene in assembly or stabilization of AChE forms that do not themselves contain a collagenous subunit. Histochemical, immunohistochemical, toxicological, and electrophysiological assays all indicated absence of AChE at ColQ-/- neuromuscular junctions. Nonetheless, neuromuscular function was initially robust, demonstrating that AChE and ColQ do not play obligatory roles in early phases of synaptogenesis. Moreover, because acute inhibition of synaptic AChE is fatal to normal animals, there must be compensatory mechanisms in the mutant that allow the synapse to function in the chronic absence of AChE. One structural mechanism appears to be a partial ensheathment of nerve terminals by Schwann cells. Compensation was incomplete, however, as animals lacking ColQ and synaptic AChE failed to thrive and most died before they reached maturity. (+info)Cloning, expression, and properties of a nonneuronal secreted acetylcholinesterase from the parasitic nematode Nippostrongylus brasiliensis. (8/2082)
We have isolated a full-length cDNA encoding an acetylcholinesterase secreted by the nematode parasite Nippostrongylus brasiliensis. The predicted protein is truncated in comparison with acetylcholinesterases from other organisms such that the carboxyl terminus aligns closely to the end of the catalytic domain of the vertebrate enzymes. The residues in the catalytic triad are conserved, as are the six cysteines which form the three intramolecular disulfide bonds. Three of the fourteen aromatic residues which line the active site gorge in the Torpedo enzyme are substituted by nonaromatic residues, corresponding to Tyr-70 (Thr), Trp-279 (Asn), and Phe-288 (Met). High level expression was obtained via secretion from Pichia pastoris. The purified enzyme behaved as a monomeric hydrophilic species. Although of invertebrate origin and possessing the above substitutions in the active site gorge residues, the enzyme efficiently hydrolyzed acetylthiocholine and showed minimal activity against butyrylthiocholine. It displayed excess substrate inhibition with acetylthiocholine at concentrations over 2. 5 mM and was highly sensitive to both active site and "peripheral" site inhibitors. Northern blot analysis indicated a progressive increase in mRNA for AChE B in parasites isolated from 6 days postinfection. (+info)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.
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.
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.
Acetylthiocholine is a synthetic chemical compound that is widely used in scientific research, particularly in the field of neuroscience. It is the acetylated form of thiocholine, which is a choline ester. Acetylthiocholine is often used as a substrate for enzymes called cholinesterases, including acetylcholinesterase (AChE) and butyrylcholinesterase (BChE).
When Acetylthiocholine is hydrolyzed by AChE, it produces choline and thioacetic acid. This reaction is important because it terminates the signal transduction of the neurotransmitter acetylcholine at the synapse between neurons. Inhibition of AChE can lead to an accumulation of Acetylthiocholine and acetylcholine, which can have various effects on the nervous system, depending on the dose and duration of inhibition.
Acetylthiocholine is also used as a reagent in the Ellman's assay, a colorimetric method for measuring AChE activity. In this assay, Acetylthiocholine is hydrolyzed by AChE, releasing thiocholine, which then reacts with dithiobisnitrobenzoic acid (DTNB) to produce a yellow color. The intensity of the color is proportional to the amount of thiocholine produced and can be used to quantify AChE activity.
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.
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.
'Electrophorus' is a scientific term that refers to a genus of electric fishes found in the Amazon River basin in South America. The name is most commonly associated with one species in particular, Electrophorus electricus, which is more popularly known as the electric eel. Despite its common name, the electric eel is not a true eel but rather a knifefish, related to catfishes and carps.
The term 'Electrophorus' comes from the Greek words "electron," meaning amber or electron (with a nod to its electrical properties), and "pherein," meaning to carry or bear. This name is fitting for the electric eel, as it has the remarkable ability to generate strong electric fields that it uses for hunting, navigation, and defense.
Electric eels possess specialized electric organs in their body, which are made up of electrocytes - cells that function like tiny batteries when stimulated. By stacking thousands of these electrocytes together, the electric eel can produce powerful electrical discharges reaching up to 600 volts and 1 ampere of current, enough to stun or even kill prey and deter potential predators.
In summary, 'Electrophorus' is a medical definition for a genus of electric fishes, with the most well-known species being the electric eel (Electrophorus electricus). These unique creatures have the ability to generate strong electric fields using specialized electric organs, which they use for hunting, navigation, and defense.
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.
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.
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.
I believe you may be mistaken when referring to "torpedo" in the context of medicine. The term "torpedo" is not typically used as a medical definition. Instead, it is a term that has various meanings in different fields such as physics, military, and anatomy (in relation to electric fishes).
However, if you are referring to the use of "torpedo" in the context of neuromuscular disorders, it may refer to a type of treatment called "neuromuscular electrical stimulation" or NMES. In this case, the term "torpedo" is used metaphorically to describe the electrical impulse that is delivered to the muscle to cause a contraction. This can be used as a therapeutic intervention for various neuromuscular conditions such as muscle weakness or paralysis.
If you have any further questions, please let me know and I will do my best to assist you!
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.
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.
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.
I'm sorry for any confusion, but "Isoflurophate" does not appear to be a recognized term in medical or scientific literature. It is possible that there may be a spelling error or typo in the term you are looking for. If you meant "Isoflurane," which is a commonly used anesthetic in medical and surgical procedures, I can provide a definition for that.
Isoflurane: A volatile halogenated ether liquid used as an inhalational general anesthetic agent. It has a rapid onset and offset of action, making it useful for both induction and maintenance of anesthesia. Isoflurane is also known to have bronchodilatory properties, which can be beneficial in patients with reactive airway disease or asthma.
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.
"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.
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.
Edrophonium is a type of medication called an anticholinesterase agent. It works by blocking the breakdown of acetylcholine, a neurotransmitter in the body that is important for muscle contraction. This results in an increase in the amount of acetylcholine available to stimulate muscle contraction.
Edrophonium is used as a diagnostic aid in the diagnosis of myasthenia gravis, a neuromuscular disorder characterized by muscle weakness and fatigue. It is also used to reverse the effects of non-depolarizing muscle relaxants, which are medications that are sometimes given during surgery to temporarily paralyze muscles.
Edrophonium is administered intravenously (through a vein) and its effects usually begin within 30 seconds to 1 minute after injection and last for about 5 to 10 minutes. Common side effects of edrophonium include sweating, increased salivation, and muscle twitching. More serious side effects, such as seizures or cardiac arrest, can occur but are rare.
It is important to note that edrophonium should only be used under the supervision of a healthcare professional, as it can cause serious side effects if not used properly.
An Electric organ is a specialized electric tissue found in some groups of fish, most notably in the electric eels and electric rays. It consists of modified muscle or nerve cells called electrocytes, which are capable of generating and transmitting electrical signals. These organs are used for various purposes such as navigation, communication, and hunting. In electric eels, for example, the electric organ can generate powerful electric shocks to stun prey or defend against predators.
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.
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.
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.
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.
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.
'Bungarus' is a genus of venomous elapid snakes commonly known as kraits, which are native to South and Southeast Asia. The term 'Bungarus' comes from the natural history classification system used in biology, specifically in the field of herpetology (the study of amphibians and reptiles).
Kraits are known for their highly potent neurotoxic venom, which can cause respiratory failure and death if left untreated. They are typically nocturnal and have a distinctive pattern of alternating black, white, and yellow bands. Some of the more well-known species in this genus include the banded krait (Bungarus fasciatus) and the Malayan krait (Bungarus candidus).
It's worth noting that 'Bungarus' is not a medical term per se, but rather a taxonomic designation used by biologists to classify a group of related organisms. However, understanding the properties and behaviors of venomous snakes like kraits can be important for medical professionals who may encounter patients who have been bitten or envenomated by these creatures.
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.
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.
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.
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.
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.
Echothiophate iodide is a cholinesterase inhibitor drug. It works by blocking the breakdown of acetylcholine, a neurotransmitter in the body that is essential for proper nerve function. By preventing the breakdown of acetylcholine, echothiophate iodide can help to improve muscle strength and reduce muscle weakness in individuals with certain neuromuscular disorders.
Echothiophate iodide is used as a diagnostic aid in ophthalmology to test for the presence and severity of glaucoma, as well as to treat certain types of glaucoma by reducing the pressure inside the eye. It is also used off-label to treat myasthenia gravis, a neuromuscular disorder characterized by muscle weakness and fatigue.
The drug is administered via injection or ophthalmic solution, depending on its intended use. Common side effects of echothiophate iodide include blurred vision, eye pain, headache, and nausea. More serious side effects can include seizures, difficulty breathing, and irregular heartbeat.
It is important to note that echothiophate iodide can interact with other medications and should be used with caution in individuals with certain medical conditions. Therefore, it is essential to consult with a healthcare provider before using this medication.
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.
Elapid venoms are the toxic secretions produced by elapid snakes, a family of venomous snakes that includes cobras, mambas, kraits, and coral snakes. These venoms are primarily composed of neurotoxins, which can cause paralysis and respiratory failure in prey or predators.
Elapid venoms work by targeting the nervous system, disrupting communication between the brain and muscles. This results in muscle weakness, paralysis, and eventually respiratory failure if left untreated. Some elapid venoms also contain hemotoxins, which can cause tissue damage, bleeding, and other systemic effects.
The severity of envenomation by an elapid snake depends on several factors, including the species of snake, the amount of venom injected, the location of the bite, and the size and health of the victim. Prompt medical treatment is essential in cases of elapid envenomation, as the effects of the venom can progress rapidly and lead to serious complications or death if left untreated.
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.
"Eels" is not a term that has a medical definition. It refers to a type of long, snake-like fish that belong to the order Anguilliformes. There are several species of eels found in fresh and saltwater environments around the world. While there may be some references to "eels" in a medical context, such as in the name of certain medical conditions or procedures, these would be specific and unrelated to the fish themselves.
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.
Malathion is a type of organophosphate pesticide that is widely used in agriculture, public health, and residential settings for the control of various insect pests. It works by inhibiting an enzyme called acetylcholinesterase, which leads to the accumulation of the neurotransmitter acetylcholine in the synapses, resulting in overstimulation of the nervous system and ultimately death of the insect.
In a medical context, malathion is also used as a topical treatment for head lice infestations. It is available in various forms, such as shampoos, lotions, and sprays, and works by killing the lice and their eggs on contact. However, it is important to follow the instructions carefully when using malathion products to avoid excessive exposure and potential health risks.
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.
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.
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.
The neuromuscular junction (NMJ) is the specialized synapse or chemical communication point, where the motor neuron's nerve terminal (presynaptic element) meets the muscle fiber's motor end plate (postsynaptic element). This junction plays a crucial role in controlling muscle contraction and relaxation.
At the NMJ, the neurotransmitter acetylcholine is released from the presynaptic nerve terminal into the synaptic cleft, following an action potential. Acetylcholine then binds to nicotinic acetylcholine receptors on the postsynaptic membrane of the muscle fiber, leading to the generation of an end-plate potential. If sufficient end-plate potentials are generated and summate, they will trigger an action potential in the muscle fiber, ultimately causing muscle contraction.
Dysfunction at the neuromuscular junction can result in various neuromuscular disorders, such as myasthenia gravis, where autoantibodies attack acetylcholine receptors, leading to muscle weakness and fatigue.
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.
Choline O-Acetyltransferase (COAT, ChAT) is an enzyme that plays a crucial role in the synthesis of the neurotransmitter acetylcholine. It catalyzes the transfer of an acetyl group from acetyl CoA to choline, resulting in the formation of acetylcholine. Acetylcholine is a vital neurotransmitter involved in various physiological processes such as memory, cognition, and muscle contraction. COAT is primarily located in cholinergic neurons, which are nerve cells that use acetylcholine to transmit signals to other neurons or muscles. Inhibition of ChAT can lead to a decrease in acetylcholine levels and may contribute to neurological disorders such as Alzheimer's disease and myasthenia gravis.
Acetylcholine is a neurotransmitter, a type of chemical messenger that transmits signals across a chemical synapse from one neuron (nerve cell) to another "target" neuron, muscle cell, or gland cell. It is involved in both peripheral and central nervous system functions.
In the peripheral nervous system, acetylcholine acts as a neurotransmitter at the neuromuscular junction, where it transmits signals from motor neurons to activate muscles. Acetylcholine also acts as a neurotransmitter in the autonomic nervous system, where it is involved in both the sympathetic and parasympathetic systems.
In the central nervous system, acetylcholine plays a role in learning, memory, attention, and arousal. Disruptions in cholinergic neurotransmission have been implicated in several neurological disorders, including Alzheimer's disease, Parkinson's disease, and myasthenia gravis.
Acetylcholine is synthesized from choline and acetyl-CoA by the enzyme choline acetyltransferase and is stored in vesicles at the presynaptic terminal of the neuron. When a nerve impulse arrives, the vesicles fuse with the presynaptic membrane, releasing acetylcholine into the synapse. The acetylcholine then binds to receptors on the postsynaptic membrane, triggering a response in the target cell. Acetylcholine is subsequently degraded by the enzyme acetylcholinesterase, which terminates its action and allows for signal transduction to be repeated.
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.
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.
Propoxur is a carbamate insecticide that acts as a cholinesterase inhibitor. It is used to control a wide variety of pests, including cockroaches, ants, fleas, and ticks. Propoxur works by disrupting the nervous system of insects, leading to paralysis and death. It can be found in various forms such as powders, granules, and liquids for use in residential and commercial settings. However, it is important to note that propoxur can also have toxic effects on non-target organisms, including humans, and its use is regulated by environmental and health agencies worldwide.
Histochemistry is the branch of pathology that deals with the microscopic localization of cellular or tissue components using specific chemical reactions. It involves the application of chemical techniques to identify and locate specific biomolecules within tissues, cells, and subcellular structures. This is achieved through the use of various staining methods that react with specific antigens or enzymes in the sample, allowing for their visualization under a microscope. Histochemistry is widely used in diagnostic pathology to identify different types of tissues, cells, and structures, as well as in research to study cellular and molecular processes in health and disease.
Insecticide resistance is a genetic selection process in insect populations that allows them to survive and reproduce despite exposure to insecticides. It's the result of changes in the genetic makeup of insects, which can be caused by natural selection when insecticides are used repeatedly. Over time, this leads to the prevalence of genes that provide resistance to the insecticide, making the pest control methods less effective. Insecticide resistance is a significant challenge in public health and agriculture, as it can reduce the efficacy of interventions aimed at controlling disease-carrying insects or protecting crops from pests.
Organothiophosphates are a class of organophosphorus compounds that contain a phosphorus atom bonded to one or more organic groups and one or more sulfur atoms. These compounds have various uses, including as plasticizers, flame retardants, and insecticides. The most well-known member of this group is the insecticide parathion. Organothiophosphates are also used in the synthesis of pharmaceuticals and other chemicals.
It's important to note that some organothiophosphates have been associated with health risks, including neurotoxicity and potential developmental effects. Therefore, their use is regulated by various government agencies around the world.
In the context of medicine and pharmacology, "kinetics" refers to the study of how a drug moves throughout the body, including its absorption, distribution, metabolism, and excretion (often abbreviated as ADME). This field is called "pharmacokinetics."
1. Absorption: This is the process of a drug moving from its site of administration into the bloodstream. Factors such as the route of administration (e.g., oral, intravenous, etc.), formulation, and individual physiological differences can affect absorption.
2. Distribution: Once a drug is in the bloodstream, it gets distributed throughout the body to various tissues and organs. This process is influenced by factors like blood flow, protein binding, and lipid solubility of the drug.
3. Metabolism: Drugs are often chemically modified in the body, typically in the liver, through processes known as metabolism. These changes can lead to the formation of active or inactive metabolites, which may then be further distributed, excreted, or undergo additional metabolic transformations.
4. Excretion: This is the process by which drugs and their metabolites are eliminated from the body, primarily through the kidneys (urine) and the liver (bile).
Understanding the kinetics of a drug is crucial for determining its optimal dosing regimen, potential interactions with other medications or foods, and any necessary adjustments for special populations like pediatric or geriatric patients, or those with impaired renal or hepatic function.
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.
A motor endplate, also known as the neuromuscular junction, is the site where a motor neuron's axon terminal synapses with a muscle fiber. It is a specialized chemical synapse that allows for the transmission of electrical signals from the nervous system to the skeletal muscles, resulting in muscle contraction. The motor endplate is composed of several structures including the presynaptic membrane, which contains neurotransmitter-filled vesicles, and the postsynaptic membrane, which contains numerous nicotinic acetylcholine receptors. When an action potential reaches the axon terminal, it triggers the release of acetylcholine into the synaptic cleft, where it binds to receptors on the postsynaptic membrane and causes the opening of ion channels, leading to the generation of an endplate potential that can trigger muscle contraction.
Aldicarb is a carbamate pesticide that acts as a systemic insecticide, nematicide, and acaricide. It is used to control a wide variety of pests in crops such as potatoes, corn, and soybeans. Aldicarb works by inhibiting the enzyme acetylcholinesterase, which leads to an accumulation of the neurotransmitter acetylcholine, causing paralysis and death in insects. However, it is highly toxic to both insects and mammals, including humans, and can cause serious health effects such as nausea, dizziness, and even death if ingested or absorbed through the skin. Therefore, its use is heavily regulated and restricted in many countries.
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.
The brain is the central organ of the nervous system, responsible for receiving and processing sensory information, regulating vital functions, and controlling behavior, movement, and cognition. It is divided into several distinct regions, each with specific functions:
1. Cerebrum: The largest part of the brain, responsible for higher cognitive functions such as thinking, learning, memory, language, and perception. It is divided into two hemispheres, each controlling the opposite side of the body.
2. Cerebellum: Located at the back of the brain, it is responsible for coordinating muscle movements, maintaining balance, and fine-tuning motor skills.
3. Brainstem: Connects the cerebrum and cerebellum to the spinal cord, controlling vital functions such as breathing, heart rate, and blood pressure. It also serves as a relay center for sensory information and motor commands between the brain and the rest of the body.
4. Diencephalon: A region that includes the thalamus (a major sensory relay station) and hypothalamus (regulates hormones, temperature, hunger, thirst, and sleep).
5. Limbic system: A group of structures involved in emotional processing, memory formation, and motivation, including the hippocampus, amygdala, and cingulate gyrus.
The brain is composed of billions of interconnected neurons that communicate through electrical and chemical signals. It is protected by the skull and surrounded by three layers of membranes called meninges, as well as cerebrospinal fluid that provides cushioning and nutrients.
Piperidines are not a medical term per se, but they are a class of organic compounds that have important applications in the pharmaceutical industry. Medically relevant piperidines include various drugs such as some antihistamines, antidepressants, and muscle relaxants.
A piperidine is a heterocyclic amine with a six-membered ring containing five carbon atoms and one nitrogen atom. The structure can be described as a cyclic secondary amine. Piperidines are found in some natural alkaloids, such as those derived from the pepper plant (Piper nigrum), which gives piperidines their name.
In a medical context, it is more common to encounter specific drugs that belong to the class of piperidines rather than the term itself.
Cholinergic receptors are a type of receptor in the body that are activated by the neurotransmitter acetylcholine. Acetylcholine is a chemical that nerve cells use to communicate with each other and with muscles. There are two main types of cholinergic receptors: muscarinic and nicotinic.
Muscarinic receptors are found in the heart, smooth muscle, glands, and the central nervous system. They are activated by muscarine, a type of alkaloid found in certain mushrooms. When muscarinic receptors are activated, they can cause changes in heart rate, blood pressure, and other bodily functions.
Nicotinic receptors are found in the nervous system and at the junction between nerves and muscles (the neuromuscular junction). They are activated by nicotine, a type of alkaloid found in tobacco plants. When nicotinic receptors are activated, they can cause the release of neurotransmitters and the contraction of muscles.
Cholinergic receptors play an important role in many physiological processes, including learning, memory, and movement. They are also targets for drugs used to treat a variety of medical conditions, such as Alzheimer's disease, Parkinson's disease, and myasthenia gravis (a disorder that causes muscle weakness).
Cholinergic fibers are nerve cell extensions (neurons) that release the neurotransmitter acetylcholine at their synapses, which are the junctions where they transmit signals to other neurons or effector cells such as muscles and glands. These fibers are a part of the cholinergic system, which plays crucial roles in various physiological processes including learning and memory, attention, arousal, sleep, and muscle contraction.
Cholinergic fibers can be found in both the central nervous system (CNS) and the peripheral nervous system (PNS). In the CNS, cholinergic neurons are primarily located in the basal forebrain and brainstem, and their projections innervate various regions of the cerebral cortex, hippocampus, thalamus, and other brain areas. In the PNS, cholinergic fibers are responsible for activating skeletal muscles through neuromuscular junctions, as well as regulating functions in smooth muscles, cardiac muscles, and glands via the autonomic nervous system.
Dysfunction of the cholinergic system has been implicated in several neurological disorders, such as Alzheimer's disease, Parkinson's disease, and myasthenia gravis.
Benzyl compounds are organic chemical compounds that contain a benzyl group, which is a functional group consisting of a carbon atom attached to a CH3 group (methyl group) and an aromatic ring, usually a phenyl group. The benzyl group can be represented as -CH2-C6H5.
Benzyl compounds have various applications in different fields such as pharmaceuticals, flavors, fragrances, dyes, and polymers. In pharmaceuticals, benzyl compounds are used as active ingredients or intermediates in the synthesis of drugs. For example, benzylpenicillin is a widely used antibiotic that contains a benzyl group.
Benzyl alcohol, benzyl chloride, and benzyl acetate are some common examples of benzyl compounds with various industrial applications. Benzyl alcohol is used as a solvent, preservative, and intermediate in the synthesis of other chemicals. Benzyl chloride is an important chemical used in the production of resins, dyes, and pharmaceuticals. Benzyl acetate is used as a flavoring agent and fragrance in food and cosmetic products.
It's worth noting that benzyl compounds can be toxic or harmful if ingested, inhaled, or come into contact with the skin, depending on their chemical properties and concentrations. Therefore, they should be handled with care and used under appropriate safety measures.
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.
Pesticides are substances or mixtures of substances intended for preventing, destroying, or repelling pests. Pests can be insects, rodents, fungi, weeds, or other organisms that can cause damage to crops, animals, or humans and their living conditions. The term "pesticide" includes all of the following: insecticides, herbicides, fungicides, rodenticides, bactericides, and various other substances used to control pests.
It is important to note that while pesticides are designed to be toxic to the target pests, they can also pose risks to non-target organisms, including humans, if not used properly. Therefore, it is essential to follow all label instructions and safety precautions when handling and applying pesticides.
A muscle is a soft tissue in our body that contracts to produce force and motion. It is composed mainly of specialized cells called muscle fibers, which are bound together by connective tissue. There are three types of muscles: skeletal (voluntary), smooth (involuntary), and cardiac. Skeletal muscles attach to bones and help in movement, while smooth muscles are found within the walls of organs and blood vessels, helping with functions like digestion and circulation. Cardiac muscle is the specific type that makes up the heart, allowing it to pump blood throughout the body.
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.
In the context of medical and biological sciences, a "binding site" refers to a specific location on a protein, molecule, or cell where another molecule can attach or bind. This binding interaction can lead to various functional changes in the original protein or molecule. The other molecule that binds to the binding site is often referred to as a ligand, which can be a small molecule, ion, or even another protein.
The binding between a ligand and its target binding site can be specific and selective, meaning that only certain ligands can bind to particular binding sites with high affinity. This specificity plays a crucial role in various biological processes, such as signal transduction, enzyme catalysis, or drug action.
In the case of drug development, understanding the location and properties of binding sites on target proteins is essential for designing drugs that can selectively bind to these sites and modulate protein function. This knowledge can help create more effective and safer therapeutic options for various diseases.
Erythrocytes, also known as red blood cells (RBCs), are the most common type of blood cell in circulating blood in mammals. They are responsible for transporting oxygen from the lungs to the body's tissues and carbon dioxide from the tissues to the lungs.
Erythrocytes are formed in the bone marrow and have a biconcave shape, which allows them to fold and bend easily as they pass through narrow blood vessels. They do not have a nucleus or mitochondria, which makes them more flexible but also limits their ability to reproduce or repair themselves.
In humans, erythrocytes are typically disc-shaped and measure about 7 micrometers in diameter. They contain the protein hemoglobin, which binds to oxygen and gives blood its red color. The lifespan of an erythrocyte is approximately 120 days, after which it is broken down in the liver and spleen.
Abnormalities in erythrocyte count or function can lead to various medical conditions, such as anemia, polycythemia, and sickle cell disease.
Nootropic agents, also known as cognition enhancers or smart drugs, are substances that are believed to improve cognitive functions such as memory, motivation, creativity, and executive functions. The term "nootropic" is derived from the Greek words "nous," meaning mind, and "tropos," meaning a turn or bend.
Nootropics can be divided into several categories, including dietary supplements, prescription medications, and illicit substances. Some examples of nootropics include:
* Piracetam and other racetams
* Caffeine and other stimulants
* Nicotine and other cholinergic compounds
* Modafinil and other wakefulness-promoting agents
* Certain antidepressants, such as fluoxetine and bupropion
* Illicit substances, such as methylphenidate (Ritalin) and amphetamines (Adderall), which are sometimes used off-label for cognitive enhancement.
It is important to note that while some nootropic agents have been shown to have cognitive benefits in certain studies, their effectiveness and safety are not fully understood. Additionally, the long-term use of some nootropics can have potential risks and side effects. Therefore, it is recommended to consult with a healthcare professional before starting any new supplement or medication regimen for cognitive enhancement.
Dimethoate is an organophosphate insecticide and acaricide (a chemical that kills mites). Its chemical formula is C5H12NO3PS. It works by inhibiting the activity of an enzyme called acetylcholinesterase, which is necessary for the proper functioning of the nervous system in both insects and mammals, including humans. This leads to an overstimulation of the nervous system, causing a variety of symptoms such as muscle twitching, tremors, convulsions, and eventually respiratory failure and death in severe cases.
Dimethoate is used to control a wide range of pests, including aphids, thrips, leafminers, and spider mites, on various crops such as fruits, vegetables, cereals, and ornamental plants. However, due to its toxicity to non-target organisms, including humans, it is important to use it with caution and follow all safety guidelines when handling and applying this chemical. It is also subject to regulations regarding its use and disposal in many countries.
Decamethonium compounds are a type of neuromuscular blocking agent used in anesthesia to induce paralysis and relaxation of skeletal muscles. These compounds work by binding to and inhibiting the action of acetylcholine receptors at the neuromuscular junction, which is the site where nerve impulses are transmitted to muscle fibers.
Decamethonium bromide is a commonly used example of a decamethonium compound. It has a rapid onset of action and causes paralysis that lasts for several minutes. This makes it useful for procedures such as endotracheal intubation, where it is important to temporarily paralyze the muscles of the throat to facilitate insertion of a breathing tube.
It's important to note that decamethonium compounds do not have any analgesic or sedative effects, so they are typically used in conjunction with other medications that provide pain relief and sedation during surgical procedures. Additionally, because these compounds can cause respiratory depression, patients must be carefully monitored and provided with mechanical ventilation as needed during their use.
Alzheimer's disease is a progressive disorder that causes brain cells to waste away (degenerate) and die. It's the most common cause of dementia — a continuous decline in thinking, behavioral and social skills that disrupts a person's ability to function independently.
The early signs of the disease include forgetting recent events or conversations. As the disease progresses, a person with Alzheimer's disease will develop severe memory impairment and lose the ability to carry out everyday tasks.
Currently, there's no cure for Alzheimer's disease. However, treatments can temporarily slow the worsening of dementia symptoms and improve quality of life.
Propidium is not a medical condition or diagnosis, but rather it is a fluorescent dye that is used in medical and scientific research. It is often used in procedures such as flow cytometry and microscopy to stain and label cells or nucleic acids (DNA or RNA). Propidium iodide is the most commonly used form of propidium, which binds to DNA by intercalating between the bases.
Once stained with propidium iodide, cells with damaged membranes will take up the dye and can be detected and analyzed based on their fluorescence intensity. This makes it possible to identify and quantify dead or damaged cells in a population, as well as to analyze DNA content and cell cycle status.
Overall, propidium is an important tool in medical research and diagnostics, providing valuable information about cell health, viability, and genetic material.
Diazonium compounds are a class of organic compounds that contain the functional group -N=N+E-, where E- represents a halide ion or an organic cation. They are typically prepared by treating an aromatic primary amine with nitrous acid (HNO2) in an acidic medium, which results in the formation of a diazonium ion.
The general reaction can be represented as follows:
R-NH2 + HNO2 + HX → R-N=N+X- + 2H2O
where R represents the aromatic ring and X- is a halide ion (Cl-, Br-, or I-).
Diazonium compounds are important intermediates in organic synthesis, particularly in the preparation of azo dyes and other colored compounds. They are also useful for introducing functional groups into aromatic rings through various chemical reactions such as sandmeyer reaction, gattermann reaction etc. However, diazonium salts are generally unstable and can decompose explosively if heated or subjected to strong shock or friction. Therefore, they must be handled with care.
Acetylcholinesterase
Acetylcholinesterase inhibitor
Cholinesterase
Proteopedia
Phenylalanine N-acetyltransferase
Enzyme inhibitor
Modes of toxic action
List of OMIM disorder codes
Minaprine
Palmatine
Cholinesterase inhibitor
Management of schizophrenia
Physostigma venenosum
Carbamate
Pesticide
Corydaline
Corydalis yanhusuo
Methiocarb
Diisopropylphosphate
N,N-Dimethyl-2-chloro-2-phenylethylamine
EA-3990
Butyrylcholine
Malathion
VX (nerve agent)
Chlorethoxyfos
EA-4056
Sleep and memory
Neuromuscular drug
Lupinine
Aquagenic pruritus
Acetylcholinesterase - Wikipedia
1MAH: Fasciculin2-Mouse Acetylcholinesterase Complex
Congenital myasthenic syndromes with acetylcholinesterase deficiency, the pathophysiological mechanisms
PRIME PubMed | Acetylcholinesterase inhibitors: structure based design, synthesis, pharmacophore modeling, and virtual screening
Steric and Dynamic Parameters Influencing In Situ Cycloadditions to Form Triazole Inhibitors with Crystalline...
PRIME PubMed | In silico Structure-based Identification of Novel Acetylcholinesterase Inhibitors Against Alzheimer's Disease
Structural Specificity of Substrates of Acetylcholinesterase | Molecular Pharmacology
Ecstasy - 3,4-methylenedioxymethamphetamine ( MDMA ) - and acetylcholinesterase activity
Current Progress in Quinazoline Derivatives as Acetylcholinesterase and Monoamine Oxidase Inhibitors - Amrita Vishwa...
Accumulation of acetylcholine receptors and acetylcholinesterase at newly formed nerve-muscle synapses. | Pharmacological...
DailyMed - NEURO 3 (oxitriptan, acetylcholinesterase human, choline chloride, dopamine, glutamic acid, glycine, histidine,...
The Diencephalon and Optic Tectum of the Longnose Gar, Lepisosteus osseus (L): Cytoarchitectonics and Distribution of...
Altered glycosylation of acetylcholinesterase in lumbar cerebrospinal fluid of patients with Alzheimer's disease | Journal of...
Binding partners for mouse acetylcholinesterase in the central nervous system - TUprints
Content Background: Inhibition of Acetylcholinesterase by Nerve Gas
QuantiChromTM Acetylcholinesterase Inhibitor Screening Kit | BioAssay Systems
NIScPR Online Periodical Repository: In vitro anti-inflammatory and acetylcholinesterase inhibition efficiency of plant...
Covalent Cross-Linking of Asymmetric Acetyl-Cholinesterase in the Extracellular Matrix of Avian Myotubes<...
Probing the origins of human acetylcholinesterase inhibition via QSAR modeling and molecular docking [PeerJ]
Identification of antiplatelet and acetylcholinesterase inhibitory constituents in betel nut
EC 3.1.1.7 - acetylcholinesterase
Esters of methanesulfonic acid as irreversible inhibitors of acetylcholinesterase. - Wikidata
acetylcholinesterases | WordFind
T3DB: Acetylcholinesterase
Central Acetylcholinesterase Inhibitor
Alzheimer Disease in Down Syndrome: Overview, Pathophysiology/Risk Factors, Epidemiology
Acetylcholinesterase | The TYP
Alzheimer Disease in Down Syndrome: Overview, Pathophysiology/Risk Factors, Epidemiology
biochemistry - Why are so many different organophosphates able to deactivate acetylcholinesterase? - Chemistry Stack Exchange
Pesticide use, erythrocyte acetylcholinesterase level and self-reported acute intoxication symptoms among vegetable farmers in...
AChE15
- This is ensured by acetylcholinesterase (AChE), which degrades ACh. (nih.gov)
- Acetylcholinesterase (AChE) is a main drug target, and its inhibitors have demonstrated functionality in the symptomatic treatment of Alzheimer's disease (AD). (unboundmedicine.com)
- Ligand binding sites on acetylcholinesterase (AChE) comprise an active center, at the base of a deep and narrow gorge lined by aromatic residues, and a peripheral site at the gorge entry. (nih.gov)
- Inhibition of acetylcholinesterase (AChE) has gained much importance since the discovery of the involvement of peripheral anionic site as an allosteric regulator of AChE. (unboundmedicine.com)
- SP - 54 EP - 68 JF - CNS & neurological disorders drug targets JO - CNS Neurol Disord Drug Targets VL - 17 IS - 1 N2 - OBJECTIVE AND BACKGROUND: Inhibition of acetylcholinesterase (AChE) has gained much importance since the discovery of the involvement of peripheral anionic site as an allosteric regulator of AChE. (unboundmedicine.com)
- METHODS: 120 MDMA abusers (MA) and 120 healthy volunteers (HV) were enrolled in an independent sample control design, in which the levels of lipoperoxide (LPO) in plasma and erythrocytes as well as the activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX) and acetylcholinesterase (AChE) in erythrocytes were determined by spectrophotometric methods. (mdma.net)
- This review mainly focuses the recent and current progresses in quinazoline derivatives as an acetylcholinesterase (AChE) and monoamine oxidase (MAO)-B inhibitors. (amrita.edu)
- The cytoarchitecture of nuclei in the diencephalon and the distribution of acetylcholinesterase (AChE) in the diencephalon and optic tectum were analyzed in the longnose gar, Lepisosteus osseus, a non-teleost actinopterygian fish. (karger.com)
- Acetylcholinesterase (AChE) is the enzyme that hydrolyses the neurotransmitter acetylcholine at the cholinergic synapses. (tu-darmstadt.de)
- Acetylcholinesterase (AChE) is an enzyme that catalyzes the breakdown of the neurotransmitter acetylcholine that is essential for cognition and memory. (peerj.com)
- To investigate the possible mechanism and the compound(s) responsible for the antiplatelet and acetylcholinesterase (AChE) inhibitory effects of Areca catechu crude extract (Ac.Cr). (jcimjournal.com)
- Zanapezil (TAK-147) is a potent, selective acetylcholinesterase (AChE) inhibitor with IC50 of 97.7 nM. (probechem.com)
- Ipidacrine hydrochloride hydrate is a reversible acetylcholinesterase (AChE) inhibitor that directly stimulates impulse transmission in the central nervous system and neuromuscular synapses by blocking membrane potassium channels. (probechem.com)
- A potent acetylcholinesterase (AChE) inhibitor with IC50 of 1.3 nM. (probechem.com)
- When administered to rats, antibodies against acetylcholinesterase (AChE) selectively destroy presynaptic inputs to sympathetic ganglia. (elsevierpure.com)
Inhibitor7
- It has also been shown that the main active ingredient in cannabis, tetrahydrocannabinol, is a competitive inhibitor of acetylcholinesterase. (wikipedia.org)
- A Cochrane review 1 included one study with a total of 10 subjects with myasthenia gravis (MG). It used acetylcholinesterase inhibitor, intranasal neostigmine, including 3 participants with ocular and 7 with generalised myasthenia gravis. (unboundmedicine.com)
- A total of 95 participants with MG were followed for 10 years to evaluate the long-term effects of prednisolone, thymectomy, or both, and compared with a group on acetylcholinesterase inhibitor (AchEI) 4 . (unboundmedicine.com)
- 1 . Mehndiratta MM, Pandey S, Kuntzer T. Acetylcholinesterase inhibitor treatment for myasthenia gravis. (unboundmedicine.com)
- Evidence Central , evidence.unboundmedicine.com/evidence/view/EBMG/457462/all/Acetylcholinesterase_inhibitor_treatment_for_myasthenia_gravis. (unboundmedicine.com)
- Donepezil is an acetylcholinesterase inhibitor that is used in dementia of the Alzheimer type. (medscape.com)
- Open up in another window Amount 4 TLC bioautography of IMM46 remove showing two substances 1 & 2 filled with the inhibitor of acetylcholinesterase, and C - control (0.1?M Galanthamine). (abt-888.net)
Inhibitors of acetylcholinesterase2
- For example, insecticides are very good inhibitors of acetylcholinesterase. (duke.edu)
- Esters of methanesulfonic acid as irreversible inhibitors of acetylcholinesterase. (wikidata.org)
Enzyme4
- Nerve gas 1 also binds to the acetylcholinesterase 2 enzyme 3 , but only at 1 site. (duke.edu)
- The body must synthesize new enzyme molecules to overcome the loss of acetylcholinesterase. (duke.edu)
- In the case of the insecticides, they don't bind to the acetylcholinesterase as tightly as does nerve gas, so the enzyme can become regenerated with time. (duke.edu)
- The short answer is that these nerve agents all share similar structural components allowing them to be bound by acetylcholinesterase, where they then either react to alter the enzyme's binding site, preventing activity, or are just very slow to hydrolyze, temporarily inhibiting the enzyme until it can remove the compound. (stackexchange.com)
Electrophorus Electricus Acetylcholinesterase1
- Barnett, P & Rosenberry, TL 1978, ' Inactivation of Electrophorus electricus acetylcholinesterase by benzenemethane sulfonylfluoride ', Archives of Biochemistry and Biophysics , vol. 190, no. 1, pp. 202-205. (elsevierpure.com)
Insensitive acetylcholinesterase1
- Conversely, more recent insensitive acetylcholinesterase resistance ( Ace1R ) genes. (cdc.gov)
Inhibition by nerve2
- As discussed in the previous section, the accumulation of acetylcholine due to acetylcholinesterase inhibition by nerve gas causes overactivation of acetylcholine receptors all over the body. (duke.edu)
- We have also identified the most probable protonation states of the active site in acetylcholinesterase before and after inhibition by nerve agents. (lu.se)
Vitro3
- Ten plant extracts were prepared and tested in in vitro assays against COX-2, COX-1 and acetylcholinesterase with evaluation of their antioxidant properties. (niscair.res.in)
- A donepezil analog that can moderately inhibit acetylcholinesterase and metal-induced Aβ aggregation in vitro and shows disassembly of Aβ aggregates. (probechem.com)
- Evaluation of their inhibition and reactivation potential in vitro showed some activity with respect to acetylcholinesterase inhibited by cyclosarin. (irb.hr)
Acetylcholine receptors1
- Accumulation of acetylcholine receptors and acetylcholinesterase at newly formed nerve-muscle synapses. (aspetjournals.org)
Inhibitory2
- In the present study, the acetylcholinesterase inhibitory property of the total extracts and fractions of Ferulago angulata and Ferulago subvelutina have been evaluated according to Ellman method. (rjpharmacognosy.ir)
- Evaluating the acetylcholinesterase inhibitory activity of Ferulago angulata and Ferulago subvelutina', Research Journal of Pharmacognosy , 1(2), pp. 39-43. (rjpharmacognosy.ir)
Irreversible1
- Benzenemethane Sulfonylfluoride (329-98-6) is an irreversible inactivator of many esterases including mammalian acetylcholinesterases. (elsevierpure.com)
Accumulation2
- The inhibition of acetylcholinesterase causes the accumulation of acetylcholine in all areas of the nervous system, causing excessive muscle contraction followed by paralysis, secretions, seizures and death by respiratory failure. (duke.edu)
- Inhibition of acetylcholinesterase leads , thereby leading to an accumulation of acetylcholine in the central and peripheral nervous system. (cdc.gov)
Sarin1
- From sarin to tricresyl phosphate , there are organophosphates that are able to deactivate acetylcholinesterase. (stackexchange.com)
Activity6
- O BJECTIVE: To investigate whether 3,4-methylenedioxymethamphetamine (MDMA) abuse produces another neurotoxicity which may significantly inhibit the acetylcholinesterase activity and result in severe oxidative damage and liperoxidative damage to MDMA abusers. (mdma.net)
- CONCLUSION: The findings in the present study suggest that MDMA abuse can induce another neurotoxicity that significantly inhibits acetylcholinesterase activity and aggravates a series of free radical chain reactions and oxidative stress in the bodies of MDMA abusers, thereby resulting in severe neural, oxidative and lipoperoxidative damages in MDMA abusers. (mdma.net)
- They contain phosphorus groups and bind avidly to acetylcholinesterase to inhibit its activity. (duke.edu)
- Acetylcholinesterase activity of one hundred and sixty one school children in the age group 15-16 years, belong to two districts, Kurunegala and Kegalle where Organophosphate and Carbamate pesticides are widely used, were studied. (who.int)
- As of today, AD patients are treated by acetylcholinesterase inhibitors which prolong cognitive function by increasing synaptic activity. (unich.it)
- Maternal caffeine exposure alters neuromotor development and hippocampus acetylcholinesterase activity in rat offspring. (bvsalud.org)
Therapeutic1
- Reactivation of inhibited acetylcholinesterase remains an important therapeutic strategy for the treatment of poisoning by organophosphorus compounds, such as nerve agents or pesticides. (irb.hr)
Substances1
- Although drugs like obidoxime or pralidoxime have been used with considerable success, there is a need for new substances capable of reactivating acetylcholinesterase with a broader scope and increased efficacy. (irb.hr)
Proteins2
- To gain an insight into the noncholinergic, cell adhesion promoting functions of acetylcholinesterase, we sought proteins interacting with it. (tu-darmstadt.de)
- This strongly suggested that the proteins encoded by these clones are binding partners of acetylcholinesterase in yeast. (tu-darmstadt.de)
Bound1
- There are some antidotes (called oxides 6 ) that could work if given fast enough, before the nerve gas becomes irreversibly bound to the acetylcholinesterase. (duke.edu)
Human1
- 1(2-Acetoxyethyl)quinuclidinium iodide has been examined as a substrate of both purified acetylcholinesterase and human serum cholinesterase. (aspetjournals.org)
Structures1
- Two distinct, but related crystal structures of the soluble, trypsin-released tetramer of acetylcholinesterase from Electrophorus electricus were solved at 4.5 and 4.2 A resolution by molecular replacement. (proteopedia.org)
Molecular1
- The stability of the ester toward acetylcholinesterase is discussed in terms of the molecular perturbation theory of drug action. (aspetjournals.org)
Binding1
- Possible screening candidates must fulfill two fundamental requirements: They must (i) show an affinity to acetylcholinesterase well balanced between sufficient binding and competitive inhibition and (ii) facilitate the nucleophilic cleavage of the phosphorylated catalytic serine residue. (irb.hr)
Effects1
- Many researches have been focused on finding new sources of medications with more potency and less side effects and investigating acetylcholinesterase inhibitors (AChEIs) has been the center of many researches. (rjpharmacognosy.ir)
Central1
- También se usan por sus efectos en el corazón y en el sistema nervioso central. (bvsalud.org)
Previous1
- However, previous reports indicated that acetylcholinesterase from the electric eel, Electrophorus electricus (EC 3.1.1.7) failed to react with benzenemethane sulfonylfluoride at measurable rates. (elsevierpure.com)
Level1
- Consequently, it is worthwhile to examine the role of anti-acetylcholinesterases in reducing the level of inflammatory markers reported in current literature. (unich.it)
Treatment1
- In myasthenia gravis the response to acetylcholinesterase inhibitors in observational studies is probably so clear that a randomised controlled trial depriving participants in a placebo arm of treatment would be difficult to justify. (unboundmedicine.com)
Cell1
- Depression of nigral pars compacta cell discharge by exogenous acetylcholinesterase. (ox.ac.uk)
Present1
- Acetylcholinesterase is present in some of the fibers in the optic tracts and in most retinorecipient nuclei, as well as in some other nuclei and tracts. (karger.com)
Role1
- There are other examples of acetylcholinesterase inhibition that play a role in our lives. (duke.edu)
Summary1
- Summary From the outcomes of our research, we conclude that acetylcholinesterase inhibitors are very prevalent in sea bacteria, specially the bacterial affiliates of sea invertebrates. (abt-888.net)