Cytochrome P-450 Enzyme System
Encyclopedias as Topic
Platelet Aggregation Inhibitors
Propachlor removal by Pseudomonas strain GCH1 in an immobilized-cell system. (1/292)A bacterial strain capable of growing on propachlor (2-chloro-N-isopropylacetanilide) was isolated from soil by using enrichment and isolation techniques. The strain isolated, designated GCH1, was classified as a member of the genus Pseudomonas. Washed-cell suspensions of strain GCH1 accumulated N-isopropylacetanilide, acetanilide, acetamide, and catechol. Pseudomonas strain GCH1 grew on propachlor with a generation time of 4.2 h and a rate of substrate utilization of 1.75 +/- 0.15 micromol h(-1). Gene expression did not require induction but was subject to catabolite expression. Acetanilide was a growth substrate with a yield of 0.56 +/- 0.02 mg of protein micromol(-1). GCH1 strain cells were immobilized by adsorption onto a ceramic support and were used as biocatalysts in an immobilized cell system. Propachlor elimination reached 98%, with a retention time of 3 h and an initial organic load of 0.5 mM propachlor. The viability of immobilized cells increased 34-fold after 120 days of bioreactor operation. (+info)
Acute metobromuron poisoning with severe associated methemoglobinemia. Identification of four metabolites in plasma and urine by LC-DAD, LC-ESI-MS, and LC-ESI-MS-MS. (2/292)A case of self poisoning with metobromuron, a urea derivative used as a herbicide, is reported. Severe methemoglobinemia observed at the admission (80%) disappeared only at day 11, and hemolysis appeared at day 4 and decreased slowly to day 12. Metobromuron was analyzed by liquid chromatography with diode-array detection. Initial plasma concentration and elimination half-life were 4.9 mg/L and 5 h, respectively. Several metabolites were also detected, and four of those were identified by liquid chromatography-electrospray mass spectrometry. Normetobromuron, bromophenylurea, and bromoacetanilide were detected in plasma, but only N-methyl bromophenylurea was detected in urine. Bromoacetanilide probably results from acetylation of the intermediate bromoaniline. Methemoglobinemia could result from metabolization of metobromuron to bromoaniline and bromoacetanilide. (+info)
Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. (3/292)Acetochlor [2-chloro-N-(ethoxymethyl)-N-(2-ethyl-6-methyl-phenyl)-acetamide], alachlor [N-(methoxymethyl)-2-chloro-N-(2, 6-diethyl-phenyl)acetamide], butachlor [N-(butoxymethyl)-2-chloro-N-(2,6-diethyl-phenyl)acetamide], and metolachlor [2-chloro-N-(2-ethyl-6-methylphenyl)-N-(2-methoxy-1-methylethyl) acetamide] are pre-emergent herbicides used in the production of agricultural crops. These herbicides are carcinogenic in rats: acetochlor and alachlor cause tumors in the nasal turbinates, butachlor causes stomach tumors, and metolachlor causes liver tumors. It has been suggested that the carcinogenicity of these compounds involves a complex metabolic activation pathway leading to a DNA-reactive dialkylbenzoquinone imine. Important intermediates in this pathway are 2-chloro-N-(2,6-diethylphenyl)acetamide (CDEPA) produced from alachlor and butachlor and 2-chloro-N-(2-methyl-6-ethylphenyl)acetamide (CMEPA) produced from acetochlor and metolachlor. Subsequent metabolism of CDEPA and CMEPA produces 2,6-diethylaniline (DEA) and 2-methyl-6-ethylaniline (MEA), which are bioactivated through para-hydroxylation and subsequent oxidation to the proposed carcinogenic product dialkylbenzoquinone imine. The current study extends our earlier studies with alachlor and demonstrates that rat liver microsomes metabolize acetochlor and metolachlor to CMEPA (0.065 nmol/min/mg and 0.0133 nmol/min/mg, respectively), whereas human liver microsomes can metabolize only acetochlor to CMEPA (0.023 nmol/min/mg). Butachlor is metabolized to CDEPA to a much greater extent by rat liver microsomes (0.045 nmol/min/mg) than by human liver microsomes (< 0.001 nmol/min/mg). We have determined that both rat and human livers metabolize both CMEPA to MEA (0.308 nmol/min/mg and 0.541 nmol/min/mg, respectively) and CDEPA to DEA (0.350 nmol/min/mg and 0.841 nmol/min/mg, respectively). We have shown that both rat and human liver microsomes metabolize MEA (0.035 nmol/min/mg and 0.069 nmol/min/mg, respectively) and DEA (0.041 nmol/min/mg and 0.040 nmol/min/mg, respectively). We have also shown that the cytochrome P450 isoforms responsible for human metabolism of acetochlor, butachlor, and metolachlor are CYP3A4 and CYP2B6. (+info)
Etidocaine, bupivacaine, and lidocaine seizure thresholds in monkeys. (4/292)The central nervous system toxicities of etidocaine, bupivacaine, and lidocaine were studied during constant-rate intravenous infusions in rhesus monkeys. Comparison of drug effects was achieved by determining the drug dosages and arterial plasma concentrations that induced electrical seizure activity. The central nervous system toxicity of etidocaine was similar to that of bupivacaine. The toxicity of each was four times greater than that of lidocaine. Since the drug infusion rates were proportional to anesthetic potencies in clinical usage, the therapeutic-toxic ratios of these three drugs are similar. (+info)
Isolation of an inducible amidase from Pseudomonas acidovorans AE1. (5/292)A bacterial strain, AEI, which hydrolysed acetanilide, was isolated from soil and identified as Pseudomonas acidovorans. Numerous amides, esters and enzyme inhibitors were tested as amidase inducers. Phenacetin was chosen as inducer for the large scale cultivation of these organisms because it was less toxic to the bacteria than acetanilide. The induction increased the enzymic activity 250-fold. In comparison, the type culture strain of P. acidovorans, ATTCCI5668, had no amidase activity which could be induced by phenacetin. Optimal growth conditions were established with respect to the concentration of carbon source and inducer so that about 10% of the extractable bacterial protein consisted of the amidase. The organisms were lysed with lysozyme in the presence of EDTA and the enzyme was isolated mainly by column chromatography procedures. A preparation form 60 g (wet wt) bacteria yielded about 100 mg highly purified amidase with a specific activity of 137 mugmol substrate hydrolysed/min/mg protien. In addition to acetanilide, the purified enzyme hydrolysed several other amides and esters. As standard substrate, p-nitroacetanilide was chosen. (+info)
Application of the PKCYP-test in cases of altered CYP1A2 for multiple CYP systems in rat models of disease. (6/292)Previously, we established a method to assess drug metabolism capacity based on a pharmacokinetic estimation of the quantity of cytochrome P450 (CYP) in vivo (PKCYP-test) by introducing an apparent liver-to-blood free concentration gradient in vivo (qg). The qg values were determined as the ratio of in vivo-in vitro clearance. In this study, we examined the application of the PKCYP-test to the clearance of acetanilide and caffeine mediated by CYP1A2 using rat models in which the levels of CYP enzymes were reduced. Rats fed a choline-deficient diet (CD-fed) and aged rats were used as models for a low level of CYP in the liver. In both rat models, the contribution (fCYP) of CYP1A2 to the in vivo intrinsic clearance values (CLint) of acetanilide and caffeine metabolism was less than unity, suggesting that other metabolic pathways are involved in the CLint. The in vivo clearance for CYP1A2 was estimated by multiplying fCYP by CLint, then the value of qg was determined as the ratio of in vivo-in vitro clearance. We predicted the level of CYP1A2 in CD-fed and aged rats, based on the clearance of acetanilide mediated by CYP1A2, using the qg value of control rats. The clearance of caffeine mediated by CYP1A2 in CD-fed and aged rats, as estimated from the predicted level of CYP1A2, correlated with the observed values. In conclusion, we have demonstrated that the PKCYP-test can be applied to CYP1A2 for drugs metabolized by multiple CYP isozymes, and/or to models involving reduced CYP. (+info)
Acetaminophen induces apoptosis of C6 glioma cells by activating the c-Jun NH(2)-terminal protein kinase-related cell death pathway. (7/292)Acetaminophen (AAP), a widely used analgesic drug, can damage various organs when taken in large doses. In this study, we investigate whether AAP causes cell damage by altering the early signaling pathways associated with cell death and survival. AAP caused time- and concentration-dependent apoptosis and DNA fragmentation of C6 glioma cells used as a model. AAP activated c-Jun N-terminal protein kinase (JNK) by 5.3-fold within 15 min. The elevated JNK activity persisted for up to 4 h before it returned to the basal level at 8 h. In contrast, activities of other mitogen-activated protein (MAP) kinases and the level of Akt phosphorylation in the cell survival pathway remained unchanged throughout the treatment. Wortmannin, an inhibitor of phosphatidylinositol-3 kinase, or SB203580, an inhibitor of p38 MAP kinase, did not reduce AAP-induced toxicity, indicating that these enzymes do not play a major role in cell toxicity. AAP-induced apoptosis was preceded by the sequential elevation of the pro-apoptotic Bax protein, cytochrome c release, and caspase-3 activity. Treatment with caspase inhibitor benzyloxycarbonyl-Asp-Glu-Val-Asp-fluoromethyl ketone (Z-DEVD-FMK) significantly reduced AAP-induced caspase-3 activation and cytotoxicity. Transfection of cDNA for the dominant-negative mutant JNK-KR or stress-activated protein kinase kinase-1 Lys-->Arg mutant (SEK1-KR), an immediate upstream kinase of JNK, significantly reduced AAP-induced JNK activation and cell death rate. The noncytotoxic analog of AAP, 3-hydroxyacetanilide, neither increased JNK activity nor caused apoptosis. Pretreatment with YH439, an inhibitor of CYP2E1 gene transcription, markedly reduced CYP2E1 mRNA, protein content, and activity, as well as the rate of AAP-induced JNK activation and cell death. These data indicate that AAP can cause cell damage by activating the JNK-related cell death pathway, providing a new mechanism for AAP-induced cytotoxicity. (+info)
Posttranslational modification of the umuD-encoded subunit of Escherichia coli DNA polymerase V regulates its interactions with the beta processivity clamp. (8/292)The Escherichia coli umuDC (pol V) gene products participate in both a DNA damage checkpoint control and translesion DNA synthesis. Interactions of the two umuD gene products, the 139-aa UmuD and the 115-aa UmuD' proteins, with components of the replicative DNA polymerase (pol III), are important for determining which biological role the umuDC gene products will play. Here we report our biochemical characterizations of the interactions of UmuD and UmuD' with the pol III beta processivity clamp. These analyses demonstrate that UmuD possesses a higher affinity for beta than does UmuD' because of the N-terminal arm of UmuD (residues 1-39), much of which is missing in UmuD'. Furthermore, we have identified specific amino acid residues of UmuD that crosslink to beta with p-azidoiodoacetanilide, defining the domain of UmuD important for the interaction. We have recently proposed a model for the solution structure of UmuD(2) in which the N-terminal arm of each protomer makes extensive contacts with the C-terminal globular domain of its intradimer partner, masking part of each surface. Taken together, our findings suggest that UmuD(2) has a higher affinity for the beta-clamp than does UmuD'(2) because of the structures of its N-terminal arms. Viewed in this way, posttranslational modification of UmuD, which entails the removal of its N-terminal 24 residues to yield UmuD', acts in part to attenuate the affinity of the umuD gene product for the beta-clamp. Implications of these structure-function analyses for the checkpoint and translesion DNA synthesis functions of the umuDC gene products are discussed. (+info)
Acetanilides are a group of chemical compounds that consist of an acetic acid molecule (CH3COO-) linked to aniline (C6H5NH2) through an amide bond (-CONH-). The most well-known member of this class is acetanilide itself (N-phenylacetamide, C8H9NO), which has been used historically as a pain reliever and fever reducer. However, its use in medicine has largely been abandoned due to the discovery of serious side effects, including the potential for causing methemoglobinemia, a condition that can lead to tissue hypoxia and even death.
Acetanilides have also been used as intermediates in the synthesis of other chemical compounds, such as dyes and pharmaceuticals. Some derivatives of acetanilide continue to be used in medicine today, including certain antipyretic and analgesic agents. However, these drugs are carefully designed and tested to minimize the risk of adverse effects associated with acetanilide itself.
Amidohydrolases are a class of enzymes that catalyze the hydrolysis of amides and related compounds, resulting in the formation of an acid and an alcohol. This reaction is also known as amide hydrolysis or amide bond cleavage. Amidohydrolases play important roles in various biological processes, including the metabolism of xenobiotics (foreign substances) and endogenous compounds (those naturally produced within an organism).
The term "amidohydrolase" is a broad one that encompasses several specific types of enzymes, such as proteases, esterases, lipases, and nitrilases. These enzymes have different substrate specificities and catalytic mechanisms but share the common ability to hydrolyze amide bonds.
Proteases, for example, are a major group of amidohydrolases that specifically cleave peptide bonds in proteins. They are involved in various physiological processes, such as protein degradation, digestion, and regulation of biological pathways. Esterases and lipases hydrolyze ester bonds in various substrates, including lipids and other organic compounds. Nitrilases convert nitriles into carboxylic acids and ammonia by cleaving the nitrile bond (C≡N) through hydrolysis.
Amidohydrolases are found in various organisms, from bacteria to humans, and have diverse applications in industry, agriculture, and medicine. For instance, they can be used for the production of pharmaceuticals, biofuels, detergents, and other chemicals. Additionally, inhibitors of amidohydrolases can serve as therapeutic agents for treating various diseases, such as cancer, viral infections, and neurodegenerative disorders.
The Cytochrome P-450 (CYP450) enzyme system is a group of enzymes found primarily in the liver, but also in other organs such as the intestines, lungs, and skin. These enzymes play a crucial role in the metabolism and biotransformation of various substances, including drugs, environmental toxins, and endogenous compounds like hormones and fatty acids.
The name "Cytochrome P-450" refers to the unique property of these enzymes to bind to carbon monoxide (CO) and form a complex that absorbs light at a wavelength of 450 nm, which can be detected spectrophotometrically.
The CYP450 enzyme system is involved in Phase I metabolism of xenobiotics, where it catalyzes oxidation reactions such as hydroxylation, dealkylation, and epoxidation. These reactions introduce functional groups into the substrate molecule, which can then undergo further modifications by other enzymes during Phase II metabolism.
There are several families and subfamilies of CYP450 enzymes, each with distinct substrate specificities and functions. Some of the most important CYP450 enzymes include:
1. CYP3A4: This is the most abundant CYP450 enzyme in the human liver and is involved in the metabolism of approximately 50% of all drugs. It also metabolizes various endogenous compounds like steroids, bile acids, and vitamin D.
2. CYP2D6: This enzyme is responsible for the metabolism of many psychotropic drugs, including antidepressants, antipsychotics, and beta-blockers. It also metabolizes some endogenous compounds like dopamine and serotonin.
3. CYP2C9: This enzyme plays a significant role in the metabolism of warfarin, phenytoin, and nonsteroidal anti-inflammatory drugs (NSAIDs).
4. CYP2C19: This enzyme is involved in the metabolism of proton pump inhibitors, antidepressants, and clopidogrel.
5. CYP2E1: This enzyme metabolizes various xenobiotics like alcohol, acetaminophen, and carbon tetrachloride, as well as some endogenous compounds like fatty acids and prostaglandins.
Genetic polymorphisms in CYP450 enzymes can significantly affect drug metabolism and response, leading to interindividual variability in drug efficacy and toxicity. Understanding the role of CYP450 enzymes in drug metabolism is crucial for optimizing pharmacotherapy and minimizing adverse effects.
Microsomes, liver refers to a subcellular fraction of liver cells (hepatocytes) that are obtained during tissue homogenization and subsequent centrifugation. These microsomal fractions are rich in membranous structures known as the endoplasmic reticulum (ER), particularly the rough ER. They are involved in various important cellular processes, most notably the metabolism of xenobiotics (foreign substances) including drugs, toxins, and carcinogens.
The liver microsomes contain a variety of enzymes, such as cytochrome P450 monooxygenases, that are crucial for phase I drug metabolism. These enzymes help in the oxidation, reduction, or hydrolysis of xenobiotics, making them more water-soluble and facilitating their excretion from the body. Additionally, liver microsomes also host other enzymes involved in phase II conjugation reactions, where the metabolites from phase I are further modified by adding polar molecules like glucuronic acid, sulfate, or acetyl groups.
In summary, liver microsomes are a subcellular fraction of liver cells that play a significant role in the metabolism and detoxification of xenobiotics, contributing to the overall protection and maintenance of cellular homeostasis within the body.
An encyclopedia is a comprehensive reference work containing articles on various topics, usually arranged in alphabetical order. In the context of medicine, a medical encyclopedia is a collection of articles that provide information about a wide range of medical topics, including diseases and conditions, treatments, tests, procedures, and anatomy and physiology. Medical encyclopedias may be published in print or electronic formats and are often used as a starting point for researching medical topics. They can provide reliable and accurate information on medical subjects, making them useful resources for healthcare professionals, students, and patients alike. Some well-known examples of medical encyclopedias include the Merck Manual and the Stedman's Medical Dictionary.
Platelet aggregation inhibitors are a class of medications that prevent platelets (small blood cells involved in clotting) from sticking together and forming a clot. These drugs work by interfering with the ability of platelets to adhere to each other and to the damaged vessel wall, thereby reducing the risk of thrombosis (blood clot formation).
Platelet aggregation inhibitors are often prescribed for people who have an increased risk of developing blood clots due to various medical conditions such as atrial fibrillation, coronary artery disease, peripheral artery disease, stroke, or a history of heart attack. They may also be used in patients undergoing certain medical procedures, such as angioplasty and stenting, to prevent blood clot formation in the stents.
Examples of platelet aggregation inhibitors include:
1. Aspirin: A nonsteroidal anti-inflammatory drug (NSAID) that irreversibly inhibits the enzyme cyclooxygenase, which is involved in platelet activation and aggregation.
2. Clopidogrel (Plavix): A P2Y12 receptor antagonist that selectively blocks ADP-induced platelet activation and aggregation.
3. Prasugrel (Effient): A third-generation thienopyridine P2Y12 receptor antagonist, similar to clopidogrel but with faster onset and greater potency.
4. Ticagrelor (Brilinta): A direct-acting P2Y12 receptor antagonist that does not require metabolic activation and has a reversible binding profile.
5. Dipyridamole (Persantine): An antiplatelet agent that inhibits platelet aggregation by increasing cyclic adenosine monophosphate (cAMP) levels in platelets, which leads to decreased platelet reactivity.
6. Iloprost (Ventavis): A prostacyclin analogue that inhibits platelet aggregation and causes vasodilation, often used in the treatment of pulmonary arterial hypertension.
7. Cilostazol (Pletal): A phosphodiesterase III inhibitor that increases cAMP levels in platelets, leading to decreased platelet activation and aggregation, as well as vasodilation.
8. Ticlopidine (Ticlid): An older P2Y12 receptor antagonist with a slower onset of action and more frequent side effects compared to clopidogrel or prasugrel.
Aspirin is the common name for acetylsalicylic acid, which is a medication used to relieve pain, reduce inflammation, and lower fever. It works by inhibiting the activity of an enzyme called cyclooxygenase (COX), which is involved in the production of prostaglandins, hormone-like substances that cause inflammation and pain. Aspirin also has an antiplatelet effect, which means it can help prevent blood clots from forming. This makes it useful for preventing heart attacks and strokes.
Aspirin is available over-the-counter in various forms, including tablets, capsules, and chewable tablets. It is also available in prescription strengths for certain medical conditions. As with any medication, aspirin should be taken as directed by a healthcare provider, and its use should be avoided in children and teenagers with viral infections due to the risk of Reye's syndrome, a rare but serious condition that can affect the liver and brain.
The placebo effect is a psychological or psychophysiological phenomenon in which a person's symptoms improve following a treatment but this improvement is not attributable to the properties of the treatment itself. Instead, it is believed to be due to the mind's belief in the effectiveness of the treatment, often influenced by positive expectations and the ritualistic aspects of the therapy itself.
Placebos are often used in clinical trials as a control group to compare against the actual treatment. The placebo effect can make it challenging to determine whether an observed improvement is truly due to the treatment or other factors.
The duodenum is the first part of the small intestine, immediately following the stomach. It is a C-shaped structure that is about 10-12 inches long and is responsible for continuing the digestion process that begins in the stomach. The duodenum receives partially digested food from the stomach through the pyloric valve and mixes it with digestive enzymes and bile produced by the pancreas and liver, respectively. These enzymes help break down proteins, fats, and carbohydrates into smaller molecules, allowing for efficient absorption in the remaining sections of the small intestine.
Platelet aggregation is the clumping together of platelets (thrombocytes) in the blood, which is an essential step in the process of hemostasis (the stopping of bleeding) after injury to a blood vessel. When the inner lining of a blood vessel is damaged, exposure of subendothelial collagen and tissue factor triggers platelet activation. Activated platelets change shape, become sticky, and release the contents of their granules, which include ADP (adenosine diphosphate).
ADP then acts as a chemical mediator to attract and bind additional platelets to the site of injury, leading to platelet aggregation. This forms a plug that seals the damaged vessel and prevents further blood loss. Platelet aggregation is also a crucial component in the formation of blood clots (thrombosis) within blood vessels, which can have pathological consequences such as heart attacks and strokes if they obstruct blood flow to vital organs.
Coronary artery bypass surgery, also known as coronary artery bypass grafting (CABG), is a surgical procedure used to improve blood flow to the heart in patients with severe coronary artery disease. This condition occurs when the coronary arteries, which supply oxygen-rich blood to the heart muscle, become narrowed or blocked due to the buildup of fatty deposits, called plaques.
During CABG surgery, a healthy blood vessel from another part of the body is grafted, or attached, to the coronary artery, creating a new pathway for oxygen-rich blood to flow around the blocked or narrowed portion of the artery and reach the heart muscle. This bypass helps to restore normal blood flow and reduce the risk of angina (chest pain), shortness of breath, and other symptoms associated with coronary artery disease.
There are different types of CABG surgery, including traditional on-pump CABG, off-pump CABG, and minimally invasive CABG. The choice of procedure depends on various factors, such as the patient's overall health, the number and location of blocked arteries, and the presence of other medical conditions.
It is important to note that while CABG surgery can significantly improve symptoms and quality of life in patients with severe coronary artery disease, it does not cure the underlying condition. Lifestyle modifications, such as regular exercise, a healthy diet, smoking cessation, and medication therapy, are essential for long-term management and prevention of further progression of the disease.
List of patent medicines
David Lester (biochemist)
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History of aspirin
Acetanilide - Wikipedia
Acetanilides | Harvard Catalyst Profiles | Harvard Catalyst
Deuteration of acetanilides and other substituted aromatics using [Ir(COD)(Cy3P)(Py)]PF6 as catalyst | RTI
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Use acetanilide in a sentence: acetanilide sentence examples
Meta Amino Acetanilide (MAA)--Taizhou Zhenhe Chemical Co., Ltd.
China good quality Peptide Powders on sales
Exploration of acetanilide derivatives of 1-(ω-phenoxyalkyl)uracils as novel inhibitors of Hepatitis C Virus replication. -...
Microsolvation of the acetanilide cation (AA(+)) in a nonpolar solvent: IR spectra of AA(+)-L-n clusters (L = He, Ar, N-2; n |=...
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Ruthenium(II)-enabled para-selective C-H difluoromethylation of anilides and their derivatives | Nature Communications
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carcinogenic agent - Ontology Report - Rat Genome Database
- However, unlike phenacetin, acetanilide and their combinations, paracetamol is not considered carcinogenic at therapeutic doses. (sentenceof.com)
- Together with Julius Axelrod, he discovered that acetanilide and phenacetin both metabolize to paracetamol. (sentenceof.com)
- Phenacetin, acetanilide , phenazone and many similar bodies act as antipyretics in virtue of an action on the heat-regulating centres in the cerebrum. (sentenceof.com)
- The unknown component is suspected to be a chemical relative of acetaminophen, either acetanilide or phenacetin. (bartleby.com)
- Medicines that can increase 5-HIAA measurements include acetaminophen (Tylenol), acetanilide, phenacetin, glyceryl guaiacolate (found in many cough syrups), methocarbamol, and reserpine. (medlineplus.gov)
- After several conflicting results over the ensuing fifty years, it was established in 1948 that acetanilide was mostly metabolized to paracetamol (acetaminophen) in the human body, and that it was this metabolite that was responsible for the analgesic and antipyretic properties. (wikipedia.org)
- Acetanilide is no longer used as a drug, although the efficacy of its metabolite paracetamol (acetaminophen) is well known. (wikipedia.org)
- The amides formed from aniline are sometimes called "anilides", for example CH 3 -CO-NH-C 6 H 5 is acetanilide . (wikidoc.org)
- It is also known as N-phenylacetamide, acetanil, or acetanilid, and was formerly known by the trade name Antifebrin. (wikipedia.org)
- Acetanilide was the first aniline derivative found to possess analgesic as well as antipyretic properties, and was quickly introduced into medical practice under the names of Antifebrin by A. Cahn and P. Hepp in 1886. (wikipedia.org)
- Antifebrin or acetanilide is obtained from acetic acid and aniline. (wikidoc.org)
- In this study, the yield of acetanilide and benzanilide synthesis and the rate of reaction were compared between the traditional heat method and microwave inducement. (sentenceof.com)
- Acetanilide can be produced by reacting acetic anhydride with aniline: C6H5NH2 + (CH3CO)2O → C6H5NHCOCH3 + CH3COOH The preparation used to be a traditional experiment in introductory organic chemistry lab classes, but it has now been widely replaced by the preparation of either paracetamol or aspirin, both of which teach the same practical techniques (especially recrystallization of the product) but which avoid the use of aniline, a suspected carcinogen. (wikipedia.org)
- According to another source a more controlled nitration of aniline starts with the formation of acetanilide by reaction with acetic anhydride followed by the actual nitration. (sentenceof.com)
- The observed methemoglobinemia after acetanilide administration was ascribed to the small proportion of acetanilide that is hydrolyzed to aniline in the body. (wikipedia.org)
- Nitroacetanilide The presence of aniline as an impurity in 19th century batches of acetanilide drugs cannot be ruled out. (wikipedia.org)
- Axelrod, J. (1948), "The estimation of acetanilide and its metabolic products, aniline, N-acetyl p-aminophenol and p-aminophenol (free and total conjugated) in biological fluids and tissues", J. Pharmacol. (wikipedia.org)
- So that to make acetanilide, for example, they no longer employed acetic acid and aniline, but they re-copulated a copulated oxalic acid with a copulated ammonia. (todayinsci.com)
- Of far greater impact was the second paper in this series, showing that paracetamol was a metabolite of acetanilide in the blood. (sentenceof.com)
- Von Mering's claims remained essentially unchallenged for half a century, until two teams of researchers from the United States analyzed the metabolism of acetanilide and paracetamol. (sentenceof.com)
- Exploration of acetanilide derivatives of 1-(ω-phenoxyalkyl)uracils as novel inhibitors of Hepatitis C Virus replication. (ox.ac.uk)
- Acetanilide is an odourless solid chemical of leaf or flake-like appearance. (wikipedia.org)
- Meta Amino Acetanilide (MAA)--Taizhou Zhenhe Chemical Co., Ltd. (clipper-ships.com)
- EULEXIN Capsules contain flutamide, an acetanilid, nonsteroidal, orally active anti- androgen having the chemical name, 2-methyl-N-[4-nitro-3 (trifluoromethyl) phenyl] propanamide. (rxlist.com)
- Infrared photodissociation (IRPD) spectra of mass-selected cluster ions of acetanilide (N-phenylacetamide), AA+-Ln, with the ligands L = He (n = 1-2), Ar (n = 1-7), and N2 (n = 1-10) are recorded in the hydride stretch (amide A, νNH, νCH) and fingerprint (amide I-III) ranges of AA+ in its 2A′′ ground electronic state. (tu-berlin.de)
- The first of these three papers summarized these theories, and reexamined the proportion of various acetanilide metabolites in human urine. (sentenceof.com)
- In the 19th century acetanilide was one of a large number of compounds used as experimental photographic developers. (wikipedia.org)
- Here, we describe new 1-(ω-phenoxyalkyl)uracils bearing acetanilide fragment in 3 position of pyrimidine ring as potential antiviral drugs against HCV. (ox.ac.uk)
- We found 14 'acetanilide' sentence examples to help you understand how to use acetanilide in a sentence . (sentenceof.com)
- Denmark Women Voting Rights During June pdf La Terms expanded come to acetanilides in Denmark. (opticasoftware.com)
- VonMuller, A trian ambassador to Japan, said he intended to spend a few weeks in this country before a i to return to Austria, Capt. JF, Erdmannsdeorffer of the Hamburg-American a pasj-eneer, c6mmanding the i Hpexla of 3,781 tons, built in 1895, was in Vladivostok when war bptwf-en Russia and Germany 'Watt declared. (newspapers.com)
- Acetanilide is also used in the preparation of thioacetamide. (peptidepowders.com)
- A bioassay for the possible carcinogenicity of 4'-(chloroacetyl)-acetanilide was conducted using Fischer 344 rats and B6C3F1 mice. (nih.gov)
- Propachlor is a pre-emergence and early post-emergence herbicide derived from acetanilide, and has been in use since 1965. (unep.org)
- 4'-(Chloroacetyl)-acetanilide, an intermediate in the synthesis of dyes and pharmaceutical compounds, was selected for bioassay by the National Cancer Institute because of the increased incidence of bladder cancer observed among dye manufacturing industry workers. (nih.gov)
- Aromatic amines, such as 4'-(chloroacetyl)-acetanilide, are among several classes of chemicals thought to contribute to the increased cancer risk in this industry, and 4'-(chloroacetyl)-acetanilide is especially suspect because it is structurally similar to the possible human renal pelvic carcinogen, phenacetin. (nih.gov)
- 4'-(Chloroacetyl)-acetanilide was administered in the feed, at either of two concentrations, to groups of 50 male and 50 female animals of each species. (nih.gov)
- There were no significant positive associations between the concentration of 4'-(chloroacetyl)-acetanilide administered and mortality in rats or mice of either sex. (nih.gov)
- Dose-related mean body weight depression was observed for males and females of both species, indicating that the concentrations of 4'-(chloroacetyl)-acetanilide administered to the animals in this bioassay may have approximated the maximum tolerated concentrations. (nih.gov)
- Under the conditions of this bioassay, 4'-(chloroacetyl)-acetanilide was not carcinogenic when administered in the diet to Fischer 344 rats or B6C3F1 mice of either sex. (nih.gov)
- for palladium(II)-catalysed synthesis of acetanilide based on carbon monoxide. (ias.ac.in)
- 8453. Adulteration and misbranding of acetanilid and salol, acetubenetidin and salol, codeine sulphate, and morpbine sulphate tablets. (nih.gov)
- In this article, Brodie and Axelrod demonstrated that acetanilide, the primary ingredient in several headache remedies, contributed to the development of the non-lethal blood condition methomoglobinemia. (nih.gov)
- Chalcones (2a-j) were synthesized from acetanilide and various aromatic aldehydes in presence of ethanol and sodium hydroxide solution. (hindawi.com)
- A method for the determination of salol and acetanilid in a mixture of the two, and of salol and acetphenetidin in their mixtures. (nih.gov)
- Adulteration and misbranding of acetanilide compound tablets. (nih.gov)
- The best weed control ratings were recorded on the DCPA (dimethyl 2,3,5,6-tetrachloroterephthalate) plus paraquat (1,1'- dimethyl-4,4'bipyridinium ion) treatment, linuron [3-(3,4-dichlorophenyl)- 1-methoxy-1-methylurea] plus paraquat treatment and the alachlor [2-chloro-2',6'-diethyl-N-(methoxy ethyl) acetanilide] plus linuron plus paraquat treatment. (tennessee.edu)
- Acetanilide is used for the production of 4-acetamidobenzenesulfonyl chloride, a key intermediate for the manufacture of the sulfa drugs. (wikipedia.org)
- Report of experiments to test the toxicity of mother's milk after administration of acetanilide. (nih.gov)
- Genetic Toxicity Evaluation of Acetanilide in Salmonella/E.coli Mutagenicity Test or Ames Test. (nih.gov)