Allylisopropylacetamide: An allylic compound that acts as a suicide inactivator of CYTOCHROME P450 by covalently binding to its heme moiety or surrounding protein.Acetamides: Derivatives of acetamide that are used as solvents, as mild irritants, and in organic synthesis.5-Aminolevulinate Synthetase: An enzyme of the transferase class that catalyzes condensation of the succinyl group from succinyl coenzyme A with glycine to form delta-aminolevulinate. It is a pyridoxyal phosphate protein and the reaction occurs in mitochondria as the first step of the heme biosynthetic pathway. The enzyme is a key regulatory enzyme in heme biosynthesis. In liver feedback is inhibited by heme. EC 2.3.1.37.Phenobarbital: A barbituric acid derivative that acts as a nonselective central nervous system depressant. It potentiates GAMMA-AMINOBUTYRIC ACID action on GABA-A RECEPTORS, and modulates chloride currents through receptor channels. It also inhibits glutamate induced depolarizations.Dicarbethoxydihydrocollidine: 1,4-Dihydro-2,4,6-trimethyl-3,5-pyridinedicarboxylic acid diethyl ester.Ethylmorphine-N-Demethylase: A drug-metabolizing enzyme of the hepatic microsomal oxidase system which catalyzes the oxidation of the N-methyl group of ethylmorphine with the formation of formaldehyde.Porphyrins: A group of compounds containing the porphin structure, four pyrrole rings connected by methine bridges in a cyclic configuration to which a variety of side chains are attached. The nature of the side chain is indicated by a prefix, as uroporphyrin, hematoporphyrin, etc. The porphyrins, in combination with iron, form the heme component in biologically significant compounds such as hemoglobin and myoglobin.MaleatesHeme: The color-furnishing portion of hemoglobin. It is found free in tissues and as the prosthetic group in many hemeproteins.Hemin: Chloro(7,12-diethenyl-3,8,13,17-tetramethyl-21H,23H-porphine-2,18-dipropanoato(4-)-N(21),N(22),N(23),N(24)) ferrate(2-) dihydrogen.Cytochrome P-450 Enzyme System: A superfamily of hundreds of closely related HEMEPROTEINS found throughout the phylogenetic spectrum, from animals, plants, fungi, to bacteria. They include numerous complex monooxygenases (MIXED FUNCTION OXYGENASES). In animals, these P-450 enzymes serve two major functions: (1) biosynthesis of steroids, fatty acids, and bile acids; (2) metabolism of endogenous and a wide variety of exogenous substrates, such as toxins and drugs (BIOTRANSFORMATION). They are classified, according to their sequence similarities rather than functions, into CYP gene families (>40% homology) and subfamilies (>59% homology). For example, enzymes from the CYP1, CYP2, and CYP3 gene families are responsible for most drug metabolism.Enzyme Induction: An increase in the rate of synthesis of an enzyme due to the presence of an inducer which acts to derepress the gene responsible for enzyme synthesis.Microsomes, Liver: Closed vesicles of fragmented endoplasmic reticulum created when liver cells or tissue are disrupted by homogenization. They may be smooth or rough.Liver: A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.

delta-Aminolevulinate synthetases in the liver cytosol fraction and mitochondria of mice treated with allylisopropylacetamide and 3,5-dicarbethoxyl-1,4-dihydrocollidine. (1/64)

Hepatic delta-aminolevulinate (ALA) synthetase was induced in mice by the administration of allylisopropylacetamide (AIA) and 3,5-dicarbethoxy-1,4-dihydrocollidine (DDC). In both cases, a significant amount of ALA synthetase accumulated in the liver cytosol fraction as well as in the mitochondria. The apparent molecular weight of the cytosol ALA synthetase was estimated to be 320,000 by gel filtration, but when the cytosol ALA synthetase was subjected to sucrose density gradient centrifugation, it showed a molecular weight of 110,000. In the mitochondria, there were two different sizes of ALA synthetase with molecular weights of 150,000 and 110,000, respectively; the larger enzyme was predominant in DDC-treated mice, whereas in AIA-treated mice and normal mice the enzyme existed mostly in the smaller form. When hemin was injected into mice pretreated with DDC, the molecular size of the mitochondrial ALA synthetase changed from 150,000 to 110,000. The half-life of ALA synthetase in the liver cytosol fraction was about 30 min in both the AIA-treated and DDC-treated mice. The half-life of the mitochondrial ALA synthetase in AIA-treated mice and normal mice was about 60 min, but in DDC-treated mice the half-life was as long as 150 min. The data suggest that the cytosol ALA synthetase of mouse liver is a protein complex with properties very similar to those of the cytosol ALA synthetase of rat liver, which has been shown to be composed of the enzyme active protein and two catalytically inactive binding proteins, and that ALA synthetase may be transferred from the liver cytosol fraction to the mitochondria with a size of about 150,000 daltons, followed by its conversion to enzyme with a molecular weight of 110,000 within the mitochondria. The process of intramitochondrial enzyme degradation seems to be affected in DDC-treated animals.  (+info)

Cytochrome CYP sources of N-alkylprotoporphyrin IX after administration of porphyrinogenic xenobiotics to rats. (2/64)

Cytochrome P-450 (CYP) 3A2 and CYP2C11 are sources of 70 and 30%, respectively, of N-vinylprotoporphyrin IX (N-vinylPP) formation after administration of 3-[(arylthio)ethyl]sydnone (TTMS) to rats. Female rats receiving TTMS were pretreated with dexamethasone, which induces CYP3A1 preferentially to CYP3A2. The resulting 12-fold increase in N-vinylPP formation showed that CYP3A1 was also a source of N-vinylPP. Phenobarbital (PB) pretreatment, which induces CYP2B1/2 and 3A1/2 in male rats, increased N-vinylPP formation after TTMS administration. Troleandomycin, a selective CYP3A inhibitor, was unable to decrease TTMS-mediated N-vinylPP formation in PB-treated male rats, indicating that CYP2B1/2 were sources of N-vinylPP. This conclusion was supported by demonstrating a 15-fold increase in TTMSinduced N-vinylPP formation in female rats after CYP2B1/2 induction with PB pretreatment. Allylispropylacetamide (AIA) inactivates rat CYP2B1/2, 2C6, 2C7, 2C11, and 3A1/2. Troleandomycin was unable to decrease N-AIA protoporphyrin IX adduct (N-AIAPP) formation, showing that CYP3A1/2 were not susceptible to AIA-mediated N-alkylation. N-AIAPP formation in females was approximately 30% of that in males, and thus we attribute 30% of N-AIAPP formation in males to the non-gender-specific isozymes (CYP2C6, 2C7, and/or 2B1/2), whereas approximately 70% originates from CYP2C11. PB treatment in female rats resulted in a 5-fold increase in N-AIAPP formation, showing that CYP2B1/2 were also susceptible to N-alkylation mediated by AIA. 1-Aminobenzotriazole elicited formation of equivalent amounts of N'N-aryl bridged protoporphyrin IX in male and female rat liver, demonstrating that nonselective mechanism-based inactivation is accompanied by nonselective conversion of the CYP heme moieties to N'N-aryl bridged protoporphyrin IX.  (+info)

On the sequence of reactions leading to cytochrome P-450 synthesis-effect of drugs. (3/64)

The effect of phenobarbital on the rates of the synthesis of the protein and heme moieties of cytochromeP-450 has been studied. For this purpose, cytochrome P-450 has been partially purified as its P-420 derivative and the labeled amino acid incorporation into the protein has been studied after subjecting a partially purified preparation to sodium dodecyl sulfate gel electrophoresis. The incorporation studies into the protein species after sodium dodecyl sulfate gel electrophoresis reveal that the drug primarily accelerates the rate of apoptotein synthesis followed by an increase in the rate of heme synthesis. The messenger for apocytochrome P-450 appears to be fairly stable.  (+info)

Cobalt stimulation of heme degradation in the liver. Dissociation of microsomal oxidation of heme from cytochrome P-450. (4/64)

The administration of cobalt to rats caused a marked increase in the oxidative degradation of heme (hematin, iron protoporphyrin-IX) BY HEPATIC MICROSOMAL ENZYMES. The onset of this enzyme stimulation was very rapid, beginning within 2 hours after injection of the metal and reaching its maximum in 16 to 24 hours. During the rapid phase of stimulation, i.e. the first 2 to 4 hours, when heme oxidation was 450% above control values, there was a significant decrease in microsomal oxidative N-demethylation activity and in microsomal oxidative Ndemethylation activity and in microsomal content of heme with an insignificant decrease in cytochrome P-450 content. Within 24 hours the oxidative activity of the microsomal electron transport chain for drugs was decreased to about 30% of the control. However, during the same period the oxidation of heme approached levels 800% above control. During this period there was a further decrease in the microsomal content of heme with a significant decrease in cytochrome P-450 content and an increase in the activity of delta-aminolevulinate synthetase. The activity of delta-aminolevulinate synthetase reached its maximum within 8 hours after cobalt treatment. Repeated injections (at 24-hour intervals) of cobalt were necessary to maintain these changes in microsomal enzyme activities since, after single injections of the metal, these parameters returned to normal within 72 hours. The inducing effect of cobalt on the oxidation of heme could be inhibited by the administration of actinomycin D and puromycin. Furthermore, this stimulatory effect could not be elicited by in vitro treatment of microsomes with cobalt nor could the effect be attributed to any soluble components of the cytoplasm. Cobalt protoporphyrin-IX was less effective than cobalt chloride in stimulating heme oxidation. 3-Amino-1, 2, 4-triazole did not enhance hepatic heme oxidation activity, while allylisopropylacetamide decreased this activity. The oxidative degradation of heme was found not to be cytochrome P-450 dependent since the highly increased levels of heme oxidation in microsomes from cobalt-treated animals could be retained despite the fact that the cytochrome P-450 content of such microsomes was decreased to spectrally undetectable amounts and drug oxidation was eliminated by treatment of the microsomes with 4 M urea. These findings exclude an obligatory role for cytochrome P-450 in the oxidation of heme compounds, although the possibility that this process is a heme-dependent oxidation is not ruled out.  (+info)

Effect of allylisopropylacetamide on Nuclear Ribonucleic Acid synthesis in rat liver. (5/64)

The porphyrogenic drug allylisopropylacetamide, a potent inducer of delta-aminolaevulinate synthetase, specifically increases nucleoplasmic RNA synthesis in rat liver. The drug-mediated increase in nucleoplasmic RNA synthesis is blocked by cycloheximide and haemin, which also inhibit the enzyme induction.  (+info)

Degradation of cytochrome P-450 haem by carbon tetrachloride and 2-allyl-2-isopropylacetamide in rat liver in vivo and in vitro. Involvement of non-carbon monoxide-forming mechanisms. (6/64)

Degradation of intrinsic hepatic [(14)C]haem was analysed as (14)CO formation in living rats and in hepatic microsomal fractions prepared from these animals 16h after pulse-labelling with 5-amino[5-(14)C]laevulinic acid, a precursor that labels bridge carbons of haem in non-erythroid tissues. NADPH-catalysed peroxidation of microsomal lipids in vitro (measured as malondialdehyde) was accompanied by loss of cytochrome P-450 and microsome-associated [(14)C]haem (largely cytochrome P-450 haem), but little (14)CO formation. No additional (14)CO was formed when carbon tetrachloride and 2-allyl-2-isopropylacetamide were added to stimulate lipid peroxidation and increase loss of cytochrome P-450 [(14)C]haem. Because the latter effect persisted despite inhibition of lipid peroxidation with MnCl(2) or phenyl-t-butylnitrone(a spin-trapping agent for free radicals), it was concluded that carbon tetrachloride, as reported for 2-allyl-2-isopropylacetamide, may promote loss of cytochrome P-450 haem through a non-CO-forming mechanism independent of lipid peroxidation. By comparison with breakdown of intrinsic haem, catabolism of [(14)C]methaemalbumin by microsomal haem oxygenase in vitro produced equimolar quantities of (14)CO and bilirubin, although these catabolites reflected only 18% of the degraded [(14)C]haem. This value was increased to 100% by addition of MnCl(2), which suggests that lipid peroxidation may be involved in degradation of exogenous haem to products other than CO. Phenyl-t-butylnitrone completely blocked haem oxygenase activity, which suggests that hydroxy free radicals may represent a species of active oxygen used by this enzyme system. After administration of carbon tetrachloride or 2-allyl-2-isopropylacetamide to labelled rats, hepatic [(14)C]haem was decreased and haem oxygenase activity was unchanged; however, (14)CO excretion was either unchanged (carbon tetrachloride) or decreased (2-allyl-2-isopropylacetamide). These changes were unaffected by cycloheximide pretreatment. From the lack of parallel losses of cytochrome P-450 [(14)C]haem and (14)CO excretion, one may infer that an important fraction of hepatic [(14)C]haem in normal rats is degraded by endogenous pathways not involving CO. We conclude that carbon tetrachloride and 2-allyl-2-isopropylacetamide accelerate catabolism of cytochrome P-450 haem through mechanisms that do not yield CO as an end product, and that are insensitive to cycloheximide and independent of haem oxygenase activity.  (+info)

Characterization of the anticonvulsant profile and enantioselective pharmacokinetics of the chiral valproylamide propylisopropyl acetamide in rodents. (7/64)

1. Propylisopropyl acetamide (PID) is a new chiral amide derivative of valproic acid. The purpose of this study was to evaluate the anticonvulsant activity of PID in rodent models of partial, secondarily generalized and sound-induced generalized seizures which focus on different methods of seizure induction, both acute stimuli, and following short-term plastic changes as a result of kindling, and to assess enantioselectivity and enantiomer-enantiomer interactions in the pharmacokinetics and pharmacodynamics of racemic PID and its pure enantiomers in rodents. 2. Anticonvulsant activity of (S)-PID, (R)-PID and racemic PID was evaluated in the 6 Hz psychomotor seizure model in mice, in the hippocampal kindled rat, and in the Frings audiogenic seizure susceptible mouse. The pharmacokinetics of (S)-PID and (R)-PID was studied in mice and rats. 3. In mice (S)-PID, (R)-PID and racemic PID were effective in preventing the 6 Hz seizures with (R)-PID being significantly (P < 0.05) more potent (ED(50) values 11 mg kg(-1), 46 mg kg(-1) and 57 mg kg(-1) at stimulation intensities of 22, 32 and 44 mA, respectively) than (S)-PID (ED(50) values 20 mg kg(-1), 73 mg kg(-1) and 81 mg kg(-1) at stimulation intensities of 22, 32 and 44 mA, respectively). (S)-PID, (R)-PID and racemic PID also blocked generalized seizures in the Frings mice (ED(50) values 16 mg kg(-1), 20 mg kg(-1) and 19 mg kg(-1) respectively). 4. In the hippocampal kindled rat a dose of 40 mg kg(-1) of (R)- and (S)-PID prevented the secondarily generalized seizure, whereas racemic PID also blocked the expression of partial seizures following an i.p. dose of 40 mg kg(-1). Racemic PID also significantly increased the seizure threshold in this model. 5. Mechanistic studies showed that PID did not affect voltage-sensitive sodium channels or kainate-, GABA- or NMDA- evoked currents. 6. The pharmacokinetics of PID was enantioselective following i.p. administration of individual enantiomers to mice, with (R)-PID having lower clearance and longer half-life than (S)-PID. In rats and mice, no enantioselectivity in the pharmacokinetics of PID was observed following administration of the racemate, which may be due to enantiomer-enantiomer interaction. 7. This study demonstrated that PID has both enantioselective pharmacokinetics and pharmacodynamics. The better anticonvulsant potency of (R)-PID in comparison to (S)-PID may be due to its more favorable pharmacokinetic profile. The enhanced efficacy of the racemate over the individual enantiomers in the kindled rat may be explained by a pharmacokinetic enantiomer-enantiomer interaction in rats. This study also showed the importance of studying the pharmacokinetics and pharmacodynamics of chiral drugs following administration of the individual enantiomers as well as the racemic mixture.  (+info)

Hepatic heme metabolism and its control. (8/64)

This review summarizes heme metabolism and focuses especially upon the control of hepatic heme biosynthesis. Activity of delta-aminolevulinic acid synthetase, the first enzyme of heme biosynthesis, is of primary importance in controlling the overall activity of this biosynthetic pathway. Delta-aminolevulinic acid synthetase is subject to inhibition and repression by heme, and numerous basic and clinical studies support the concept that there exists within hepatocytes a "regulatory" heme pool which controls activity of delta-aminolevulinic acid synthetase. In addition, activity of this enzyme is repressed by feeding, especially by ingestion of carbohydrates (the so-called "glucose effect"). Studies pertaining to the mechanisms underlying this effect are also reviewed. The "glucose effect" appears to be mediated by glucose or perhaps by glucose-6-phosphate or uridine diphosphate glucose, rather than by metabolites further removed from glucose itself. Unlike the situation in E. coli, the "glucose effect" in liver of higher organisms is not mediated by alterations in intracellular concentrations of cyclic AMP. Effects of heavy metals, especially iron, on hepatic heme metabolism are also considered. Iron has been found to inhibit formation and utilization of uroporphyrinogen III and to lead to decreased concentrations of microsomal heme and cytochrome P-450. Administration of large amounts of iron is also associated with an increase in activity of heme oxygenase, a property shared by several other metal ions, most notably cobalt. This effect of iron or cobalt administration is similar to the effect of heme administration in increasing heme oxygenase activity; however, we believe it is unlikely that iron, rather than heme itself, is a physiologic regulator of hepatic heme metabolism, although this hypothesis has lately been proposed.  (+info)

*Aminolevulinic acid synthase

... (ALA synthase, ALAS, or delta-aminolevulinic acid synthase) is an enzyme (EC 2.3.1.37) that catalyzes the synthesis of D-aminolevulinic acid (ALA) the first common precursor in the biosynthesis of all tetrapyrroles such as hemes, cobalamins and chlorophylls. The reaction is as follows: succinyl-CoA + glycine ⇌ {\displaystyle \rightleftharpoons } δ-aminolevulinic acid + CoA + CO2 This enzyme is expressed in all non-plant eukaryotes and the α-class of proteobacteria. Other organisms produce ALA through a three enzyme pathway known as the Shemin pathway. ALA is synthesized through the condensation of glycine and succinyl-CoA. In humans, transcription of ALA synthase is tightly controlled by the presence of Fe2+-binding elements, to prevent accumulation of porphyrin intermediates in the absence of iron. There are two forms of ALA synthase in the body. One form is expressed in red blood cell precursor cells (ALAS2), whereas the other (ALAS1) is ubiquitously expressed ...

*Translocator protein

... (TSPO) is an 18 kDa protein mainly found on the outer mitochondrial membrane. It was first described as peripheral benzodiazepine receptor (PBR), a secondary binding site for diazepam, but subsequent research has found the receptor to be expressed throughout the body and brain. In humans, the translocator protein is encoded by the TSPO gene. It belongs to family of tryptophan-rich sensory proteins. Regarding intramitochondrial cholesterol transport, TSPO has been proposed to interact with StAR (steroidogenic acute regulatory protein) to transport cholesterol into mitochondria, though evidence is mixed. In animals, TSPO (PBR) is a mitochondrial protein usually located in the outer mitochondrial membrane and characterised by its ability to bind a variety of benzodiazepine-like drugs, as well as to dicarboxylic tetrapyrrole intermediates of the haem biosynthetic pathway. TSPO has many proposed functions depending on the tissue. The most studied of these include roles in the ...

*Aminolevulinic acid synthase

... (ALA synthase, ALAS, or delta-aminolevulinic acid synthase) is an enzyme (EC 2.3.1.37) that catalyzes the synthesis of D-aminolevulinic acid (ALA) the first common precursor in the biosynthesis of all tetrapyrroles such as hemes, cobalamins and chlorophylls. The reaction is as follows: succinyl-CoA + glycine ⇌ {\displaystyle \rightleftharpoons } δ-aminolevulinic acid + CoA + CO2 This enzyme is expressed in all non-plant eukaryotes and the α-class of proteobacteria. Other organisms produce ALA through a three enzyme pathway known as the Shemin pathway. ALA is synthesized through the condensation of glycine and succinyl-CoA. In humans, transcription of ALA synthase is tightly controlled by the presence of Fe2+-binding elements, to prevent accumulation of porphyrin intermediates in the absence of iron. There are two forms of ALA synthase in the body. One form is expressed in red blood cell precursor cells (ALAS2), whereas the other (ALAS1) is ubiquitously expressed ...

*Aminolevulinic acid

δ-Aminolevulinic acid (also dALA, δ-ALA, 5ALA or 5-aminolevulinic acid), an endogenous non-protein amino acid, is the first compound in the porphyrin synthesis pathway, the pathway that leads to heme in mammals and chlorophyll in plants. 5ALA is used in photo dynamic detection and photo dynamic surgery of cancer. Being a precursor of photosensitizer, 5ALA is also used as an agent for photodynamic therapy. Photodynamic detection is the use of photosensitive drugs with a light source of the right wavelength for the detection of cancer, using fluorescence of the drug. 5ALA, or derivatives thereof, can be used to visualize bladder cancer by fluorescence imaging. It elicits synthesis and accumulation of fluorescent porphyrins (protoporphyrin IX) in epithelia and neoplastic tissues, among them malignant gliomas. It is used to visualise tumorous tissue in neurosurgical procedures. Studies since 2006 have shown that the intraoperative use of this guiding method may reduce the tumour residual volume ...

*Pearson syndrome

... is a mitochondrial disease characterized by sideroblastic anemia and exocrine pancreas dysfunction. Other clinical features are failure to thrive, pancreatic fibrosis with insulin-dependent diabetes and exocrine pancreatic deficiency, muscle and neurologic impairment, and, frequently, early death. It is usually fatal in infancy. The few patients who survive into adulthood often develop symptoms of Kearns-Sayre syndrome. It is caused by a deletion in mitochondrial DNA. Pearson syndrome is very rare, less than hundred cases have been reported in medical literature worldwide. The syndrome was first described by pediatric hematologist and oncologist Howard Pearson in 1979; the deletions causing it were discovered a decade later. Pearson Syndrome is a very rare mitochondrial disorder that is characterized by health conditions such as sideroblastic anemia, liver disease, and exocrine pancreas deficiency. Pearson Syndrome is a mitochondrial disease caused by a deletion in mitochondrial ...

*Constitutive androstane receptor

The constitutive androstane receptor (CAR) also known as nuclear receptor subfamily 1, group I, member 3 is a protein that in humans is encoded by the NR1I3 gene. CAR is a member of the nuclear receptor superfamily and along with pregnane X receptor (PXR) functions as a sensor of endobiotic and xenobiotic substances. In response, expression of proteins responsible for the metabolism and excretion of these substances is upregulated. Hence, CAR and PXR play a major role in the detoxification of foreign substances such as drugs. Androstenol and several isomers of androstanol, androstanes, are endogenous antagonists of the CAR, and despite acting as antagonists, were the basis for the naming of this receptor. More recently, dehydroepiandrosterone (DHEA), also an androstane, has been found to be an endogenous agonist of the CAR. CAR is a member of the nuclear receptor superfamily, and is a key regulator of xenobiotic and endobiotic metabolism. Unlike most nuclear receptors, this transcriptional ...

*Cyclopentobarbital

... sodium (Cyclopal, Dormisan) is a barbiturate derivative invented in the 1940s.[1] It has sedative and anticonvulsant properties, and was used primarily as an anaesthetic in veterinary medicine.[2] Cyclopal is considered similar in effects to phenobarbital but lasts almost three times as long, and is considered a long-acting barbiturate with a fairly slow onset of action.. ...

*Corvalol

... (Корвалол, Corvalolum, Korvalol)® is a mild tranquilizer based on valerian (herb) root and phenobarbital, popular in Eastern Europe and the former Soviet Union as a heart medication. It is available as a transparent liquid with a characteristic strong aroma, and as white bi-concave scored tablets. While not available for sale in the Western countries, Corvalol is sometimes brought over from Eastern Europe for self-administration to other countries of residence. Corvalol contains documented amounts of psychoactive chemicals, and may interact with other prescription medications that a person is taking. Corvalol is labeled by the manufacturer for use in Neuroses with heightened irritability Insomnia As a part of complex treatment of hypertension Non-acute spasm of coronary vessels Tachycardia Gastrointestinal cramping (as a spasmolytic agent) Valerian (herb) extract (a component of corvalol) has been historically used for insomnia and conditions associated with anxiety. It has ...

*Feniletilmalonamide

Il feniletilmalonamide (o PEMA, dall'inglese Phenylethylmalonamide) è un metabolita attivo minore del primidone. Dopo somministrazione per via endovenosa il feniletilmalonamide si distribuisce molto rapidamente nell'organismo. A seguito di somministrazione orale PEMA è facilmente assorbito dal tratto gastrointestinale. Il picco di concentrazione sierica si verifica entro 2-4 ore e la biodisponibilità orale si aggira tra l'86% e il 95,9%. L'emivita varia tra le 17 e le 25 ore. L'emivita nel paziente anziano è considerevolmente più lunga, quasi il doppio rispetto ai pazienti più giovani, in un range compreso tra le 30,7 e le 57,9 ore. Il farmaco viene eliminato principalmente immodificato nelle urine. Come farmaco il feniletilmalonamide è stato studiato per la terapia del tremore essenziale. In letteratura esistono diverse segnalazioni di sovradosaggio da primidone, ma sono rare le intossicazioni in cui si dimostrano livelli ematici elevati del suo principale metabolita, la ...

*Aminolevulinic acid synthase

... (ALA synthase, ALAS, or delta-aminolevulinic acid synthase) is an enzyme (EC 2.3.1.37) that catalyzes the synthesis of D-aminolevulinic acid (ALA) the first common precursor in the biosynthesis of all tetrapyrroles such as hemes, cobalamins and chlorophylls. The reaction is as follows: succinyl-CoA + glycine ⇌ {\displaystyle \rightleftharpoons } δ-aminolevulinic acid + CoA + CO2 This enzyme is expressed in all non-plant eukaryotes and the α-class of proteobacteria. Other organisms produce ALA through a three enzyme pathway known as the Shemin pathway. ALA is synthesized through the condensation of glycine and succinyl-CoA. In humans, transcription of ALA synthase is tightly controlled by the presence of Fe2+-binding elements, to prevent accumulation of porphyrin intermediates in the absence of iron. There are two forms of ALA synthase in the body. One form is expressed in red blood cell precursor cells (ALAS2), whereas the other (ALAS1) is ubiquitously expressed ...

*Fires of Rebellion

... é um filme mudo norte-americano de 1917, do gênero drama, dirigido por Ida May Park, estrelado por Lon Chaney e distribuído pela Universal. Dorothy Phillips - Madge Garvey William Stowell - John Blake Lon Chaney - Russell Hanlon Belle Bennett - Helen Mallory Golda Madden - Cora Hayes Alice May Youse - Sra. Garvey Ed Brady - Dan Mallory Dick La Reno - Joe Garvey (como Richard La Reno) «Fires of Rebellion». Silent Era. Consultado em 5 de agosto de 2014 «Fires of Rebellion». lonchaney.org. Consultado em 5 de agosto de 2014 Janiss Garza, Rovi. «Review Summary: Fires of Rebellion (1917)». NYTimes.com. Consultado em 5 de agosto de 2014 Fires of Rebellion (em inglês) no Internet Movie Database Portal do ...

*Ethylmorphine

... (also known as codethyline, dionine, and ethyl morphine) is an opioid analgesic and antitussive. Codeine Dihydrocodeine Morphine Pholcodine Xu, Bang Qian; Aasmundstad, Tor A.; Lillekjendlie, Bjern; Bjørneboe, Anders; Christophersen, Asbjørg S.; Mørland, Jørg (April 1997). "Effects of Ethanol on Ethylmorphine Metabolism in Isolated Rat Hepatocytes: Characterization by Means of a Multicompartmental Model". Pharmacology & Toxicology. 80 (4): 171-181. doi:10.1111/j.1600-0773.1997.tb00392.x. ISSN 1600-0773. PMID 9140136. Jonasson, B.; Jonasson, U.; Holmgren, P.; Saldeen, T. (August 1999). "Fatal poisonings where ethylmorphine from antitussive medications contributed to death". International Journal of Legal Medicine. 112 (5): 299-302. doi:10.1007/s004140050253. ISSN 1437-1596. PMID 10460420. Popa, Cornelia; Beck, Olof; Brodin, Kerstin (March-April 1998). "Morphine Formation from Ethylmorphine: Implications for Drugs-of-Abuse Testing in Urine". Journal of Analytical Toxicology. 22 ...

*Talaporfin

... (INN, also known as aspartyl chlorin, mono-L-aspartyl chlorin e6, NPe6, or LS11) is a photosensitizer used in photodynamic therapy (PDT). It absorbs red light at 664-667 nm normally provided by a laser tuned to this wavelength. It was approved in Japan (in 2004) for PDT of lung cancer and marketed as Laserphyrin. It is trademarked as Aptocine by Light Sciences Oncology. http://journals.lww.com/jto/Fulltext/2006/06000/Photodynamic_Therapy__PDT__for_Lung_Cancers.18.aspx "Photodynamic Therapy (PDT) for Lung Cancers" 2006 http://meeting.ascopubs.org/cgi/content/abstract/24/18_suppl/7229 "Photodynamic therapy using Laserphyrin for centrally located early stage lung cancer" 2006 http://www.lsoncology.com/aptocine Extracorporeal Photo-Immunotherapy for Circulating Tumor ...
Cultured chick embryo hepatocytes were iron-loaded with ferric nitrilotriacetate. Iron-loading was confirmed by both quantitative cellular iron determinations and ultrastructural studies. With iron-loading, lipid peroxidation, as detected by malonaldehyde released into the medium, occurred at a linear rate for 12h, after which time the rate of malonaldehyde production decreased. No cell toxicity, as detected by lactate dehydrogenase release, was noted. The amount of malonaldehyde recovered in the medium after 18h of exposure to iron represented 24-33% of the total malonaldehyde that could be produced by incubating lysed cells with iron and ascorbate. Cellular glutathione was not affected by iron-stimulated lipid peroxidation, but was increased by allylisopropylacetamide. Although iron-loading by itself had no effect on activity of 5-aminolaevulinate synthase, the first and rate-limiting step in haem synthesis, iron-loading in the presence of the porphyrogenic drug allylisopropylacetamide ...
An allylic compound that acts as a suicide inactivator of CYTOCHROME P450 by covalently binding to its heme moiety or surrounding protein ...
Endotoxin was administered to rats at a dose shown previously to stimulate hepatic haem oxygenase activity and to block induction of delta-aminolaevulinate synthase, apparently by causing redistribution of haem from cytochrome P-450 to a regulatory haem pool in the liver. Within 5h of the administration of endotoxin (at a time when the effect of the compound on cytochrome P-450 is maximal) the relative saturation of tryptophan pyrrolase with intrinsic haem rose, from a basal value of 50% to 90%, indicating that free haem had become available. Concurrently, the activity of delta-aminolaevulinate synthase was decreased to 25% of its basal value. Haem oxygenase reached peak activity 13h after endotoxin administration. These findings provide new evidence for the existence of an unassigned hepatic haem fraction, which exchanges with cytochrome P-450 haem and regulates these three enzyme functions. ...
Peter W. F. Fischer, Ph.D., Aida Ferizovic, B.Sc., Ian R. Neilson, B.Sc., Gerald S. Marks, D.Phil.; Porphyrin-inducing Activity of Alfaxolone and Alfadolone Acetate in Chick Embryo Liver Cells. Anesthes 1979;50(4):350-352. Download citation file:. ...
78109-65-6 - ANQNNBDIHLKZCC-UHFFFAOYSA-N - Barbituric acid, 5-allyl-1-benzyl-3-(2-(dimethylamino)ethyl)-5-isopropyl-, hydrochloride - Similar structures search, synonyms, formulas, resource links, and other chemical information.
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An improved procedure was developed for the isolation of rat alveolar type-II cells, and the properties of cytochrome-P450 dependent monoxygenase activity expressed as the O-dealkylation of four alkoxyphenoxazones (ROPh) in cells from control and beta- naphthoflavone (BNF) treated rats were examined. The specificity of the effect of BNF on P450 dependent enzyme activity was also studied. Ethoxyphe
1-Allyl-3-(2-hydroxyethyl)-2-thiourea - CAS-RN:[105-81-7] - N-allyl-n-(2-hydroxyethyl)thiourea; Otava-bb 5012538; 1-(2-Hydroxyethyl)-3-(prop-2-en-1-yl)thiourea
MetabolismBiosynthesis of cofactors, prosthetic groups, and carriersHeme, porphyrin, and cobalamin5-aminolevulinic acid synthase (TIGR01821; EC 2.3.1.37; HMM-score: 285.7) ...
MetabolismBiosynthesis of cofactors, prosthetic groups, and carriersHeme, porphyrin, and cobalamin5-aminolevulinic acid synthase (TIGR01821; EC 2.3.1.37; HMM-score: 184.5) ...
Consequences of genetic polymorphisms in Cytochrome P450 2C9 for pharmacokinetics and effects of Diclofenac and Ibuprofen. Cytochrome-P450 2C9 is considered to catalyse the 4-hydroxylation of the nonsteroidal analgesic drug diclofenac and the hydroxylation of S-ibuprofen in humans. There are two variants of Cyp2C9. Their impact on diclofenac/ ibuprofen pharmacokinetics and on the inhibition of cyclooxygenases 1 and 2 was studied in 21 healthy volunteers with all combinations of the Cyp2C9 variants *2 and *3. Blood concentrations of diclofenac/ racemic ibuprofen (and of S-ibuprofen and R-ibuprofen) were measured by HPLC. Thromboxane B2 and prostaglandin E2 were measured with use of an enzyme immunoassay. There was no evidence of impaired metabolism of diclofenac in heterozygous and homozygous carriers of the Cyp2C9 alleles *2 and *3 compared to the wildtype. Furthermore, plasma concentrations of the metabolite 4-OH-diclofenac were not lower in carriers of Cyp2C9*2 and *3. Marked diclofenac ...
The Archaeological Institute of America (AIA) is the oldest and largest archaeological organization in North America. The AIA seeks to educate people of all ages about the significance of archaeological discovery. For more than a century the AIA has been dedicated to the encouragement and support of archaeological research and publication, and to the protection of the worlds archaeological resources and cultural heritage. By traveling on an AIA Tour you directly support the AIA while personally gaining the benefit of the AIAs network of scholars and worldwide contacts.. ...
The Archaeological Institute of America (AIA) is the oldest and largest archaeological organization in North America. The AIA seeks to educate people of all ages about the significance of archaeological discovery. For more than a century the AIA has been dedicated to the encouragement and support of archaeological research and publication, and to the protection of the worlds archaeological resources and cultural heritage. By traveling on an AIA Tour you directly support the AIA while personally gaining the benefit of the AIAs network of scholars and worldwide contacts.. ...
The AUAs Clinical Practice Guidelines provide evidence-based guidance with an explicit clinical scope and purpose. AUA also provides Policy Statements, Best Practice Statements, Position Statements and White Papers to provide urology professionals with the best in peer-reviewed treatment recommendations and research.
Reference: Samsonova M.L., Oksenkrug G.F., Inhibition by monoamine oxidase inhibitors of substrate induction of liver tryptophan pyrrolase and increase in brain serotonin, Voprosy meditsinskoi khimii, 1972, vol: 18(2), 198-202 ...
Institute of Sports Medicine The Third Hospital Peking University Beijing 100083 China 2 Department of Cell Biology Capital University of Medical Sciences Beijing 100054 China To investigate whether the expression of exogenous heme oxygenase 1 HO 1 gene within vascular smooth muscle cells VSMC could protect the cells from free radical attack and inhibit cell proliferation we established an in vitro transfection of human HO 1 gene into rat VSMC mediated by a retroviral vector The results showed that the profound expression of HO 1 protein as well as HO activity was 1 8 and 2 0 fold increased respectively in the transfected cells compared to the non transfected ones The treatment of VSMC with different concentrations of H 2 O 2 led to the remarkable cell damage as indicated by survival rate and LDH leakage However the resistance of the HO 1 transfected VSMC against H 2 O 2 was significantly raised This protective effect was dramatically diminished when the transfected VSMC were pretreated with ...
Subcellular Localization of Iron and Heme Metabolism Related Proteins at Early Stages of Erythrophagocytosis. . Biblioteca virtual para leer y descargar libros, documentos, trabajos y tesis universitarias en PDF. Material universiario, documentación y tareas realizadas por universitarios en nuestra biblioteca. Para descargar gratis y para leer online.
2-(4-Allyl-3-pyridin-3-yl-5-thioxo-4,5-dihydro-[1,2,4]triazol-1-yl)-6,8-dioxa-bicyclo[3.2.1]octan-4-one | C16H16N4O3S | CID 535453 - structure, chemical names, physical and chemical properties, classification, patents, literature, biological activities, safety/hazards/toxicity information, supplier lists, and more.
This guide provides details about the overall migration strategy, process, and utilities used to migrate from Oracle Application Integration Architecture (AIA) 2.
Aminolevulinic acid synthase (ALA synthase, ALAS, or delta-aminolevulinic acid synthase) is an enzyme (EC 2.3.1.37) that catalyzes the synthesis of D-aminolevulinic acid (ALA) the first common precursor in the biosynthesis of all tetrapyrroles such as hemes, cobalamins and chlorophylls. The reaction is as follows: succinyl-CoA + glycine ⇌ {\displaystyle \rightleftharpoons } δ-aminolevulinic acid + CoA + CO2 This enzyme is expressed in all non-plant eukaryotes and the α-class of proteobacteria. Other organisms produce ALA through a three enzyme pathway known as the Shemin pathway. ALA is synthesized through the condensation of glycine and succinyl-CoA. In humans, transcription of ALA synthase is tightly controlled by the presence of Fe2+-binding elements, to prevent accumulation of porphyrin intermediates in the absence of iron. There are two forms of ALA synthase in the body. One form is expressed in red blood cell precursor cells (ALAS2), whereas the other (ALAS1) is ubiquitously expressed ...
Several xenobiotics caused hepatic porphyrin accumulation through mechanism-based inactivation of cytochrome P450(P450) and heme alkylation. Loss of iron from the alkylated heme results in formation of an N-alkylporphyrin, which is a potent inhibitor of ferrochelatase. N-Vinylprotoporphyrin IX (N-vinylPP) was identified in chick embryo liver after in ovo administration of 3-[(arylthio)ethyl]sydnone (TTMS). Pretreatment of chick embryos with beta-naphthoflavone, which causes a 90-fold increase in P450 1A levels, did not increase the formation of N-vinylPP after TTMS administration, showing that the heme moiety of P450 1A does not contribute to the formation of N-vinylPP. Increased amounts of N-vinylPP were isolated from dexamethasone-, phenobarbital-, and glutethimide-pretreated chick embryos, and it is possible that P450 2H and/or a P450 3A-like isozyme contributes to the formation of N-vinylPP. The ring B-substituted (NB) regioisomer of N-vinylPP constituted the lowest percentage of the total ...
R-H + 1/2 O2 -----, R- OH. Such reactions are imperative for the elimination of harmful hydrophobic compounds such as steroid precursors and pesticides. This reaction is of great interest to many industries, in particular the petroleum industry, which produces thousands of tons of alkanes per annum. These industries have a limited usage for alkanes and they are therefore compounds of low value. Thus, companies like Sasol are interested in the partial oxidation of alkanes , which will produce fine chemicals of high value such as alcohols, ketones and aldehydes.. Intensive research has been undertaken during the past few decades using synthetic iron porphyrins as models of the Cytochrome-P450 enzymes. A large amount of success has been achieved using porphyrins with good turnover rates, yields and selectivity on an industrial scale. Phthalocyanines have the same chemical behaviour as the naturally occurring porphyrins, with an added advantage of stability and ease of production. We plan to study ...
Allyl-(4,6-bis-dimethylamino-[1,3,5]triazin-2-yl)-cyanamide | C11H17N7 | CID 750966 - structure, chemical names, physical and chemical properties, classification, patents, literature, biological activities, safety/hazards/toxicity information, supplier lists, and more.
The inducing action of hydrocortisone and L-tryptophan on hepatic tryptophan pyrrolase in rats treated previously with CCl4 was studied. CCl4 exhibited a dose-dependent (and time-dependent) inhibitory action on the hematin-activated (apoenzyme) form of tryptophan pyrrolase but had no effect on basal holoenzyme activity. A low dose of CCl4 (0.1 ml/kg) abolished induction of the holoenzyme by hydrocortisone but had little effect on the tryptophan-induced holoenzyme or total enzyme activity. This inhibitory action of CCl4 required between 6 and 12 hr of exposure of the animal to CCl4 in vivo, i.e., prior to administration of the inducing agents. A 10-fold increase in CCl4 dose to 1.0 ml/kg did not abolish the inducing action of tryptophan; however, the enzyme response to tryptophan administration was appreciably reduced in rats receiving the higher CCl4 dose.. ...
2 major biochemical reactions that occur in the peroxisome is the mixed function oxidase and the other is a catalase but what 2 enzymes are involved in these reactions?...beta oxidation one of them ...

Iron loading of cultured hepatocytes. Effect of iron on 5-aminolaevulinate synthase is independent of lipid peroxidation |...Iron loading of cultured hepatocytes. Effect of iron on 5-aminolaevulinate synthase is independent of lipid peroxidation |...

Cellular glutathione was not affected by iron-stimulated lipid peroxidation, but was increased by allylisopropylacetamide. ... but did potentiate an increase in 5-aminolaevulinate synthase on exposure to allylisopropylacetamide. It therefore appears that ... iron-loading in the presence of the porphyrogenic drug allylisopropylacetamide increased levels of 5-aminolaevulinate synthase ...
more infohttp://www.biochemj.org/content/212/2/321

Inhibition of the Acute Toxicity and Adrenocorticolytic Effect of 7,12-Dimethylbenz(a)anthracene by Isopropylvaleramide and...Inhibition of the Acute Toxicity and Adrenocorticolytic Effect of 7,12-Dimethylbenz(a)anthracene by Isopropylvaleramide and...

Isopropylvaleramide (IVA) and allylisopropylacetamide (AIA) inhibit hemorrhagic adrenocortical necrosis and mortality caused by ... anthracene by Isopropylvaleramide and Allylisopropylacetamide in the Rat. Arpad Somogyi, Wayne Levin, Sipra Banerjee, Ronald ... anthracene by Isopropylvaleramide and Allylisopropylacetamide in the Rat ... anthracene by Isopropylvaleramide and Allylisopropylacetamide in the Rat ...
more infohttp://cancerres.aacrjournals.org/content/35/9/2500

Kinetics and metabolism of 2,2-diethylallylacetamide in dog and man | SpringerLinkKinetics and metabolism of 2,2-diethylallylacetamide in dog and man | SpringerLink

Doedens, D. J.: Metabolic fate of the porphyrinogenic drug allylisopropylacetamide. Ph.D. Thesis, Univ. of Illinois, U.S.A., ...
more infohttps://link.springer.com/article/10.1007/BF00586590

The EPA National Library Catalog | EPA National Library Network | US EPAThe EPA National Library Catalog | EPA National Library Network | US EPA

Allylisopropylacetamide Induces Rat Hepatic Ornithine Decarboxylase (Journal Version).. Author. Kitchin, K. T. ; Brown, J. L. ... Allylisopropylacetamide ; Ornithine decarboxylase ; Porphyrinogens ; Enzyme induction ; Liver ; Laboratory animals ; Amides ; ...
more infohttps://cfpub.epa.gov/ols/catalog/advanced_bibliography.cfm?FIELD1=AUTHOR&INPUT1=BROWN%20AND%20A.%20AND%20J.&TYPE1=ALL&LOGIC1=AND&COLL=&SORT_TYPE=MTIC&start_row=10

Mkrtchian S[au] - PubMed - NCBIMkrtchian S[au] - PubMed - NCBI

Hemin-mediated restoration of allylisopropylacetamide-inactivated CYP2B1: a role for glutathione and GRP94 in the heme-protein ...
more infohttps://www.ncbi.nlm.nih.gov/pubmed?cmd=search&term=Mkrtchian+S%5Bau%5D&dispmax=50

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             - Vrije Universiteit AmsterdamFind Research Outputs - Vrije Universiteit Amsterdam

Influence of allylisopropylacetamide and phenobarbital treatment on in vivo antipyrine metabolite formation in rats. Teunissen ... INFLUENCE OF ALLYLISOPROPYLACETAMIDE AND PHENOBARBITAL TREATMENT ON INVIVO ANTIPYRINE METABOLITE FORMATION IN RATS. TEUNISSEN, ...
more infohttps://research.vu.nl/en/publications/?format=&page=2963

An investigation into the hepatic cytochrome P-450 catalysed metabolism of the anaesthetic fluroxene (2,2,2-trifluoroethyl...An investigation into the hepatic cytochrome P-450 catalysed metabolism of the anaesthetic fluroxene (2,2,2-trifluoroethyl...

The role of the different cytochromes P-450 in the metabolism of the anaesthetic agent fluroxene, and the mechanism of production of toxic effects seen after pre-treatment of the animals with pehnobarbital prior to anaesthesia, have been investigated. Male rats were anaesthetized with fluroxene, or with 2,2,2-trifluroethyl ethyl ether, or with ethyl vinyl ether in an attempt to ascertain the in vivo toxic effects of the three anaesthetic agents. The resultant hepatic histology is reported. A study of the binding and metabolism of fluroxene by isolated rat hepatic microsomes was also made. We conclude that it is elevated levels of cytochrome P-450 which potentiate the toxicity of fluroxene anaesthesia in phenobarbital treated animals and that cytochrome P-448 does not bind or metabolize fluroxene. The potential toxicity of the fluroxene molecule is considered to reside in the trifluoroethyl moiety, while the vinyl group of fluroxene appears to play a role in the observed liver damage.
more infohttps://www.meta.org/papers/an-investigation-into-the-hepatic-cytochrome-p-450/1863

Acyclic Acids (Ethanoic Acids)  < Carboxylic Acids  << Organic Compounds (Organic Chemicals)  <<< Compounds, Elements & more  @...Acyclic Acids (Ethanoic Acids) < Carboxylic Acids << Organic Compounds (Organic Chemicals) <<< Compounds, Elements & more @...

Allylisopropylacetamide *Iodoacetamide *Linezolid *Piracetam *Thioacetamide *Acetic Acid *Potassium Acetate *Sodium Acetate * ...
more infohttp://wellnessadvocate.com/?uid=84521

Pyridines. Medical searchPyridines. Medical search

Hepatic delta-aminolevulinate (ALA) synthetase was induced in mice by the administration of allylisopropylacetamide (AIA) and 3 ... delta-Aminolevulinate synthetases in the liver cytosol fraction and mitochondria of mice treated with allylisopropylacetamide ...
more infohttps://lookformedical.com/en/search/pyridines

List of MeSH codes (D02) - WikipediaList of MeSH codes (D02) - Wikipedia

... allylisopropylacetamide MeSH D02.241.081.038.108.400 --- iodoacetamide MeSH D02.241.081.038.108.650 --- piracetam MeSH D02.241. ... allylisopropylacetamide MeSH D02.455.326.271.367 --- ethylenes MeSH D02.455.326.271.367.300 --- dichloroethylenes MeSH D02.455. ... allylisopropylacetamide MeSH D02.065.064.294 --- benzeneacetamides MeSH D02.065.064.294.088 --- bufexamac MeSH D02.065.064.400 ...
more infohttps://en.wikipedia.org/wiki/List_of_MeSH_codes_(D02)

Items where Year is 1975ePrints@IIScItems where Year is [email protected]

Sardana, MK and Rao, MR Satyanarayana and Padmanaban, G (1975) Effect of allylisopropylacetamide on Nuclear Ribonucleic Acid ...
more infohttp://eprints.iisc.ac.in/view/year/1975.default.html

Items where Year is 1975 - ePrints@IIScItems where Year is 1975 - [email protected]

Sardana, MK and Rao, MR Satyanarayana and Padmanaban, G (1975) Effect of allylisopropylacetamide on Nuclear Ribonucleic Acid ...
more infohttp://eprints.iisc.ernet.in/view/year/1975.default.html

Hodgson E.   A Textbook of Modern Toxicology :: ?????????   ?????????? ??????????????  ????   ??????  ??Hodgson E. A Textbook of Modern Toxicology :: ????????? ?????????? ?????????????? ???? ?????? ??

Allylisopropylacetamide 185 189 Altitude, metabolic effects 200 Aluminum 318 Alveolar ducts 317 Alveoli 317 American conference ...
more infohttp://lib.mexmat.ru/books/3602

Liste alphabétique			- TermSciences
		Liste alphabétique - TermSciences

Consultation de terminologies scientifiques multilingues (définitions, traductions multilingues, synonymes, classifications, termes associés ou spécifiques ou génériques)
more infohttp://inserm.termsciences.fr/-/Index/Explorer/Alphabet/

ALLYLISOPROPYLACETAMIDE (CAS No. 299-78-5) Suppliers @ ChemicalRegister.comALLYLISOPROPYLACETAMIDE (CAS No. 299-78-5) Suppliers @ ChemicalRegister.com

Allylisopropylacetamide; Allylisopropylacetamide (porphyria inducer) Molecular Formula: C8H15NO. Molecular Weight: 141.210800 [ ... ALLYLISOPROPYLACETAMIDE (CAS No. 299-78-5) Suppliers. Limit companies to: Worldwide USA China India ...
more infohttps://www.chemicalregister.com/ALLYLISOPROPYLACETAMIDE/Suppliers/pid849405.htm

Kinetic studies of the N-demethylation of ethylmorphine by a cytochrome P-450-dependent enzyme system in human liver microsomes...Kinetic studies of the N-demethylation of ethylmorphine by a cytochrome P-450-dependent enzyme system in human liver microsomes...

Differential haemin-mediated restoration of cytochrome P -450 N -demethylases after inactivation by allylisopropylacetamide ... containing haem or cobalt-protoporphyrin in liver homogenates of rats treated with phenobarbital and allylisopropylacetamide ...
more infohttps://portlandpress.com/biochemj/article-abstract/122/1/30P/4960/Kinetic-studies-of-the-N-demethylation-of

ConceptNet 5: allylConceptNet 5: allyl

en allylisopropylacetamide (n) ➜ * en allylnickel (n) ➜ * en allyloxy (n) ➜ * en allylpalladium (n) ➜ ...
more infohttp://conceptnet.media.mit.edu/c/en/allyl

Biochemical Effects of the Porphyrinogenic Drug Allyisopropylacetamide ePrints@IIScBiochemical Effects of the Porphyrinogenic Drug Allyisopropylacetamide [email protected]

Successive administrations of allylisopropylacetamide, a potent porphyrinogenic drug, increase liver weight, microsomal protein ... Again, phenobarbital does not share the property of allylisopropylacetamide in causing an initial decrease in cytochrome P-450 ... Haematin does not counteract most of the biochemical effects caused by allylisopropylacetamide, although it is quite effective ... Haematin does not inhibit the uptake of [2-(14)C]allylisopropylacetamide by any of the liver subcellular fractions. ...
more infohttp://eprints.iisc.ac.in/28719/

Biochemical effects of 3,5-diethoxycarbonyl-1, 4-dihydrocollidine in mouse liver ePrints@IIScBiochemical effects of 3,5-diethoxycarbonyl-1, 4-dihydrocollidine in mouse liver [email protected]

The biochemical effects of the drug are compared and discussed with those reported for allylisopropylacetamide and ...
more infohttp://eprints.iisc.ac.in/23129/

Items where Year is 1975ePrints@IIScItems where Year is [email protected]

Sardana, MK and Rao, MR Satyanarayana and Padmanaban, G (1975) Effect of allylisopropylacetamide on Nuclear Ribonucleic Acid ...
more infohttp://eprints.iisc.ac.in/view/year/1975.html
  • Doedens, D. J.: Metabolic fate of the porphyrinogenic drug allylisopropylacetamide. (springer.com)
  • Although iron-loading by itself had no effect on activity of 5-aminolaevulinate synthase, the first and rate-limiting step in haem synthesis, iron-loading in the presence of the porphyrogenic drug allylisopropylacetamide increased levels of 5-aminolaevulinate synthase 6-fold over levels induced by the drug alone. (biochemj.org)
  • Phenobarbital, which has been reported to exhibit all these changes mentioned, is a weaker inducer of delta-aminolaevulinate synthetase and increases the rate of haem synthesis only after a considerable time-lag in fed female rats, when compared with the effects observed with allylisopropylacetamide. (iisc.ac.in)
  • Again, phenobarbital does not share the property of allylisopropylacetamide in causing an initial decrease in cytochrome P-450 content. (iisc.ac.in)
  • Haematin does not counteract most of the biochemical effects caused by allylisopropylacetamide, although it is quite effective in the case of phenobarbital. (iisc.ac.in)
  • The biochemical effects of the drug are compared and discussed with those reported for allylisopropylacetamide and phenobarbital. (iisc.ac.in)
  • Successive administrations of allylisopropylacetamide, a potent porphyrinogenic drug, increase liver weight, microsomal protein and phospholipid contents. (iisc.ac.in)