An antilipemic agent that is the biologically active metabolite of CLOFIBRATE.
A fibric acid derivative used in the treatment of HYPERLIPOPROTEINEMIA TYPE III and severe HYPERTRIGLYCERIDEMIA. (From Martindale, The Extra Pharmacopoeia, 30th ed, p986)
An enzyme localized predominantly within the plasma membrane of lymphocytes. It catalyzes the transfer of long-chain fatty acids, preferentially unsaturated fatty acids, to lysophosphatides with the formation of 1,2-diacylglycero-3-phosphocholine and CoA. EC 2.3.1.23.
A lipid-regulating agent that lowers elevated serum lipids primarily by decreasing serum triglycerides with a variable reduction in total cholesterol.
An enzyme that catalyzes the formation of oleoyl-CoA, A, and water from stearoyl-CoA, AH2, and oxygen where AH2 is an unspecified hydrogen donor.
A fatty acid coenzyme derivative which plays a key role in fatty acid oxidation and biosynthesis.
Electron-dense cytoplasmic particles bounded by a single membrane, such as PEROXISOMES; GLYOXYSOMES; and glycosomes.
An antilipemic agent that lowers CHOLESTEROL and TRIGLYCERIDES. It decreases LOW DENSITY LIPOPROTEINS and increases HIGH DENSITY LIPOPROTEINS.
A peroxisome proliferator that is used experimentally to promote liver tumors. It has been used as an antihyperlipoproteinemic agent.
Compounds that either share the structure of fibric acid in their molecular arrangement or are considered variants of the fibric acid structure.
An enzyme that catalyzes the first and rate-determining steps of peroxisomal beta-oxidation of fatty acids. It acts on COENZYME A derivatives of fatty acids with chain lengths from 8 to 18, using FLAVIN-ADENINE DINUCLEOTIDE as a cofactor.
An antilipemic agent which reduces both CHOLESTEROL and TRIGLYCERIDES in the blood.
A family of enzymes that catalyze the stereoselective, regioselective, or chemoselective syn-dehydrogenation reactions. They function by a mechanism that is linked directly to reduction of molecular OXYGEN.
A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.
A flavoprotein oxidoreductase that has specificity for medium-chain fatty acids. It forms a complex with ELECTRON TRANSFERRING FLAVOPROTEINS and conveys reducing equivalents to UBIQUINONE.
Substances that lower the levels of certain LIPIDS in the BLOOD. They are used to treat HYPERLIPIDEMIAS.
Oxidoreductases that are specific for KETONES.
Closed vesicles of fragmented endoplasmic reticulum created when liver cells or tissue are disrupted by homogenization. They may be smooth or rough.
A ketone oxidoreductase that catalyzes the overall conversion of alpha-keto acids to ACYL-CoA and CO2. The enzyme requires THIAMINE DIPHOSPHATE as a cofactor. Defects in genes that code for subunits of the enzyme are a cause of MAPLE SYRUP URINE DISEASE. The enzyme was formerly classified as EC 1.2.4.3.
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.
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.
Organic, monobasic acids derived from hydrocarbons by the equivalent of oxidation of a methyl group to an alcohol, aldehyde, and then acid. Fatty acids are saturated and unsaturated (FATTY ACIDS, UNSATURATED). (Grant & Hackh's Chemical Dictionary, 5th ed)
A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.
The study of ENVIRONMENTAL POLLUTION and the toxic effects of ENVIRONMENTAL POLLUTANTS on the ECOSYSTEM. The term was coined by Truhaut in 1969.
The unstable triatomic form of oxygen, O3. It is a powerful oxidant that is produced for various chemical and industrial uses. Its production is also catalyzed in the ATMOSPHERE by ULTRAVIOLET RAY irradiation of oxygen or other ozone precursors such as VOLATILE ORGANIC COMPOUNDS and NITROGEN OXIDES. About 90% of the ozone in the atmosphere exists in the stratosphere (STRATOSPHERIC OZONE).
An array of tests used to determine the toxicity of a substance to living systems. These include tests on clinical drugs, foods, and environmental pollutants.
The univalent radical OH. Hydroxyl radical is a potent oxidizing agent.
A branch of engineering concerned with the design, construction, and maintenance of environmental facilities conducive to public health, such as water supply and waste disposal.
Analgesic antipyretic derivative of acetanilide. It has weak anti-inflammatory properties and is used as a common analgesic, but may cause liver, blood cell, and kidney damage.
A phenolphthalein that is used as a diagnostic aid in hepatic function determination.
Glycosides of GLUCURONIC ACID formed by the reaction of URIDINE DIPHOSPHATE GLUCURONIC ACID with certain endogenous and exogenous substances. Their formation is important for the detoxification of drugs, steroid excretion and BILIRUBIN metabolism to a more water-soluble compound that can be eliminated in the URINE and BILE.
Derivatives of GLUCURONIC ACID. Included under this heading are a broad variety of acid forms, salts, esters, and amides that include the 6-carboxy glucose structure.
Proteins involved in the transport of organic anions. They play an important role in the elimination of a variety of endogenous substances, xenobiotics and their metabolites from the body.
A bile pigment that is a degradation product of HEME.
Educational institutions providing facilities for teaching and research and authorized to grant academic degrees.
Liquid, solid, or gaseous waste resulting from mining of radioactive ore, production of reactor fuel materials, reactor operation, processing of irradiated reactor fuels, and related operations, and from use of radioactive materials in research, industry, and medicine. (McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed)
A group of cold-blooded, aquatic vertebrates having gills, fins, a cartilaginous or bony endoskeleton, and elongated bodies covered with scales.
Solution titration in which the end point is read from the electrode-potential variations with the concentrations of potential determining ions. (From McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed)
Electrodes which can be used to measure the concentration of particular ions in cells, tissues, or solutions.
A polyvinyl resin used extensively in the manufacture of plastics, including medical devices, tubing, and other packaging. It is also used as a rubber substitute.
The homogeneous mixtures formed by the mixing of a solid, liquid, or gaseous substance (solute) with a liquid (the solvent), from which the dissolved substances can be recovered by physical processes. (From Grant & Hackh's Chemical Dictionary, 5th ed)
The determination of the concentration of a given component in solution (the analyte) by addition of a liquid reagent of known strength (the titrant) until an equivalence point is reached (when the reactants are present in stoichiometric proportions). Often an indicator is added to make the equivalence point visible (e.g., a change in color).
Electric conductors through which electric currents enter or leave a medium, whether it be an electrolytic solution, solid, molten mass, gas, or vacuum.
A nuclear transcription factor. Heterodimerization with RETINOID X RECEPTOR GAMMA is important to metabolism of LIPIDS. It is the target of FIBRATES to control HYPERLIPIDEMIAS.
Intracellular receptors that can be found in the cytoplasm or in the nucleus. They bind to extracellular signaling molecules that migrate through or are transported across the CELL MEMBRANE. Many members of this class of receptors occur in the cytoplasm and are transported to the CELL NUCLEUS upon ligand-binding where they signal via DNA-binding and transcription regulation. Also included in this category are receptors found on INTRACELLULAR MEMBRANES that act via mechanisms similar to CELL SURFACE RECEPTORS.
A nuclear transcription factor. Heterodimerization with RETINOID X RECEPTOR ALPHA is important in regulation of GLUCOSE metabolism and CELL GROWTH PROCESSES. It is a target of THIAZOLIDINEDIONES for control of DIABETES MELLITUS.
TRANSCRIPTION FACTORS that are activated by ligands and heterodimerize with RETINOID X RECEPTORS and bind to peroxisome proliferator response elements in the promoter regions of target genes.
Tools or devices for generating products using the synthetic or chemical conversion capacity of a biological system. They can be classical fermentors, cell culture perfusion systems, or enzyme bioreactors. For production of proteins or enzymes, recombinant microorganisms such as bacteria, mammalian cells, or insect or plant cells are usually chosen.
Any of several processes in which undesirable impurities in water are removed or neutralized; for example, chlorination, filtration, primary treatment, ion exchange, and distillation. It includes treatment of WASTE WATER to provide potable and hygienic water in a controlled or closed environment as well as provision of public drinking water supplies.
The discarding or destroying of liquid waste products or their transformation into something useful or innocuous.
A phylum of bacteria consisting of the purple bacteria and their relatives which form a branch of the eubacterial tree. This group of predominantly gram-negative bacteria is classified based on homology of equivalent nucleotide sequences of 16S ribosomal RNA or by hybridization of ribosomal RNA or DNA with 16S and 23S ribosomal RNA.
Artificially produced membranes, such as semipermeable membranes used in artificial kidney dialysis (RENAL DIALYSIS), monomolecular and bimolecular membranes used as models to simulate biological CELL MEMBRANES. These membranes are also used in the process of GUIDED TISSUE REGENERATION.
Refuse liquid or waste matter carried off by sewers.
Elimination of ENVIRONMENTAL POLLUTANTS; PESTICIDES and other waste using living organisms, usually involving intervention of environmental or sanitation engineers.

Effect of cryopreservation on cytochrome P-450 enzyme induction in cultured rat hepatocytes. (1/224)

In the present study, we evaluated the inducibility of cytochrome P-450 (CYP) CYP1A, CYP2B, CYP3A, and CYP4A by beta-naphthoflavone, phenobarbital, dexamethasone, and clofibric acid, respectively, in primary hepatocyte cultures prepared from both fresh and cryopreserved rat hepatocytes. Rat hepatocytes were successfully thawed and cultured after cryopreservation in liquid nitrogen for up to 1 month. Percentage of total recovery, viable cell recovery, and final viability of the cells were 68%, 72%, and 85%, respectively. Regardless of whether they were cryopreserved or not, cultured hepatocytes exhibited near-normal morphology. Treatment of cryopreserved hepatocytes with beta-naphthoflavone caused an 8-fold increase in 7-ethoxyresorufin O-dealkylase (CYP1A1/2) activity, with an EC50 of 1.5 microM; treatment with phenobarbital caused a 26-fold increase in 7-pentoxyresorufin O-dealkylase (CYP2B1/2) activity, with an EC50 of 10 microM; treatment with dexamethasone caused a 10-fold increase in testosterone 6beta-hydroxylase (CYP3A1/2) activity, with an EC50 of 1.3 microM, whereas treatment with clofibric acid caused a 3-fold increase in lauric acid 12-hydroxylase (CYP4A1-3) activity, with an EC50 of 170 microM. The induction of CYP1A, CYP2B, CYP3A, and CYP4A enzymes by these inducers was confirmed by Western immunoblotting. The patterns of P-450 induction in cryopreserved rat hepatocytes, in terms of concentration response, reproducibility, magnitude, and specificity of response, were similar to those observed in freshly isolated hepatocytes. Additionally, the magnitude and specificity of induction was similar to that observed in vivo in rats. In conclusion, under the conditions examined, cryopreserved rat hepatocytes appear to be a suitable in vitro system for evaluating xenobiotics as inducers of P-450 enzymes.  (+info)

Insulin differentially affects xenobiotic-enhanced, cytochrome P-450 (CYP)2E1, CYP2B, CYP3A, and CYP4A expression in primary cultured rat hepatocytes. (2/224)

Uncontrolled diabetes results in enhanced expression of cytochrome P-450 (CYP)2E1, CYP2B, CYP3A, and CYP4A. Because of the simultaneous and confounding metabolic and hormonal changes that occur in vivo as a consequence of diabetes, primary cultured rat hepatocytes provide an excellent model system for examination of the effects of insulin on P-450 expression and on xenobiotic-mediated P-450 expression. In the present study, we examined the effects of insulin on pyridine-, phenobarbital-, and ciprofibrate-mediated expression of CYP2E1, CYP2B, CYP3A, and CYP4A in primary cultured rat hepatocytes. Pyridine addition to primary rat hepatocytes cultured in the presence of 1 nM insulin or in the absence of insulin resulted in a 3.5-fold and 3-fold enhancement in CYP2E1 protein expression, respectively, in the absence of any pyridine-mediated increase in mRNA expression. In contrast, hepatocytes cultured in the standard concentration of 1 microM insulin resulted in only a 2-fold increase in protein expression. Thus, the fold-induction of CYP2E1 protein in response to pyridine was 1.5- to 1.8-fold greater in either the absence of insulin or in the presence of 1 nM insulin, respectively, than that monitored in the presence of 1 microM insulin. To examine whether insulin effects on xenobiotic-mediated CYP2E1 expression were selective, insulin effects on xenobiotic-mediated expression of transcriptionally regulated CYP2B, CYP3A, and CYP4A were examined. Pyridine- or phenobarbital-mediated induction of CYP2B mRNA and protein expression in hepatocytes was suppressed by as much as 80% at lower insulin levels (0 and 1 nM), relative to the level monitored in the presence of 1 microM insulin. Omitting insulin from the medium resulted in a 50% decrease in CYP3A mRNA levels in response to phenobarbital treatment and a 30% decrease in CYP4A mRNA levels in response to ciprofibrate treatment, relative to the level obtained in response to these treatments in the presence of 1 microM insulin. The results of this study demonstrate that decreasing the insulin level in the primary hepatocyte culture medium enhanced xenobiotic-mediated CYP2E1 expression, whereas lower insulin levels suppressed xenobiotic-mediated CYP2B, CYP3A, and CYP4A expression in this cell culture system.  (+info)

Fibrates suppress fibrinogen gene expression in rodents via activation of the peroxisome proliferator-activated receptor-alpha. (3/224)

Plasma fibrinogen levels have been identified as an important risk factor for cardiovascular diseases. Among the few compounds known to lower circulating fibrinogen levels in humans are certain fibrates. We have studied the regulation of fibrinogen gene expression by fibrates in rodents. Treatment of adult male rats with fenofibrate (0.5% [wt/wt] in the diet) for 7 days decreased hepatic Aalpha-, Bbeta-, and gamma-chain mRNA levels to 52% +/- 7%, 46% +/- 8%, and 81% +/- 19% of control values, respectively. In parallel, plasma fibrinogen concentrations were decreased to 63% +/- 7% of controls. The suppression of fibrinogen expression was dose-dependent and was already evident after 1 day at the highest dose of fenofibrate tested (0.5% [wt/wt]). Nuclear run-on experiments showed that the decrease in fibrinogen expression after fenofibrate occurred at the transcriptional level, as exemplified for the gene for the Aalpha-chain. Other fibrates tested showed similar effects on fibrinogen expression and transcription. The effect of fibrates is specific for peroxisome proliferator-activated receptor-alpha (PPARalpha) because a high-affinity ligand for PPARgamma, the thiazolidinedione BRL 49653, lowered triglyceride levels, but was unable to suppress fibrinogen expression. Direct evidence for the involvement of PPARalpha in the suppression of fibrinogen by fibrates was obtained using PPARalpha-null (-/-) mice. Compared with (+/+) mice, plasma fibrinogen levels in (-/-) mice were significantly higher (3.20 +/- 0.48 v 2.67 +/- 0.42 g/L). Also, hepatic fibrinogen Aalpha-chain mRNA levels were 25% +/- 11% higher in the (-/-) mice. On treatment with 0.2% (wt/wt) fenofibrate, a significant decrease in plasma fibrinogen to 77% +/- 10% of control levels and in hepatic fibrinogen Aalpha-chain mRNA levels to 65% +/- 12% of control levels was seen in (+/+) mice, but not in (-/-) mice. These studies show that PPARalpha regulates basal levels of plasma fibrinogen and establish that fibrate-suppressed expression of fibrinogen in rodents is mediated through PPARalpha.  (+info)

The effect of peroxisome proliferators on mitochondrial bioenergetics. (4/224)

Peroxisome proliferators are a group of structurally diverse chemicals that cause the proliferation of peroxisomes in rodents. The purpose of this investigation was to test the hypothesis that the shared effect of these compounds on peroxisome proliferation is mediated through a common inhibitory effect on mitochondrial bioenergetics. Freshly isolated rat liver mitochondria were energized with succinate. The effect of the chemicals on mitochondrial bioenergetics was analyzed by monitoring calcium-induced changes in membrane potential and swelling, as well as changes in mitochondrial respiration. Mitochondrial membrane potential was measured with a TPP(+)-sensitive electrode, and swelling was recorded spectrophotometrically. Mitochondrial oxygen uptake was monitored with a Clark-type oxygen electrode. Gemfibrozil and WY-14,643 induced the mitochondrial permeability transition as characterized by calcium-induced swelling and depolarization of membrane potential, both of which were inhibited by cyclosporine A. Fenofibrate, clofibrate, ciprofibrate and diethylhexyl phthalate, on the other hand, caused a direct dose-dependent depolarization of mitochondrial membrane potential. However, the mechanism of membrane depolarization varied among the test chemicals. Bezafibrate and trichloroethylene elicited no effect on succinate-supported mitochondrial bioenergetics. The results of this investigation demonstrate that although most, but not all, peroxisome proliferators interfere with mitochondrial bioenergetics, the specific biomolecular mechanism differs among the individual compounds.  (+info)

Absence of spontaneous peroxisome proliferation in enoyl-CoA Hydratase/L-3-hydroxyacyl-CoA dehydrogenase-deficient mouse liver. Further support for the role of fatty acyl CoA oxidase in PPARalpha ligand metabolism. (5/224)

Peroxisomes contain a classical L-hydroxy-specific peroxisome proliferator-inducible beta-oxidation system and also a second noninducible D-hydroxy-specific beta-oxidation system. We previously generated mice lacking fatty acyl-CoA oxidase (AOX), the first enzyme of the L-hydroxy-specific classical beta-oxidation system; these AOX-/- mice exhibited sustained activation of peroxisome proliferator-activated receptor alpha (PPARalpha), resulting in profound spontaneous peroxisome proliferation in liver cells. These observations implied that AOX is responsible for the metabolic degradation of PPARalpha ligands. In this study, the function of enoyl-CoA hydratase/L-3-hydroxyacyl-CoA dehydrogenase (L-PBE), the second enzyme of this peroxisomal beta-oxidation system, was investigated by disrupting its gene. Mutant mice (L-PBE-/-) were viable and fertile and exhibited no detectable gross phenotypic defects. L-PBE-/- mice showed no hepatic steatosis and manifested no spontaneous peroxisome proliferation, unlike that encountered in livers of mice deficient in AOX. These results indicate that disruption of classical peroxisomal fatty acid beta-oxidation system distal to AOX step does not interfere with the inactivation of endogenous ligands of PPARalpha, further confirming that the AOX gene is indispensable for the physiological regulation of this receptor. The absence of appreciable changes in lipid metabolism also indicates that enoyl-CoAs, generated in the classical system in L-PBE-/- mice are diverted to D-hydroxy-specific system for metabolism by D-PBE. When challenged with a peroxisome proliferator, L-PBE-/- mice showed increases in the levels of hepatic mRNAs and proteins that are regulated by PPARalpha except for appreciable blunting of peroxisome proliferative response as compared with that observed in hepatocytes of wild type mice similarly treated. This blunting of peroxisome proliferative response is attributed to the absence of L-PBE protein in L-PBE-/- mouse liver, because all other proteins are induced essentially to the same extent in both wild type and L-PBE-/- mice.  (+info)

Hepatic hyperplasia and cancer in rats: alterations in copper metabolism. (6/224)

We previously demonstrated that rats exposed to the peroxisome proliferator (PP) diethylhexylphthalate (DEHP) had reduced serum ceruloplasmin (CP) oxidase activity, which suggests tissue copper deposition. Copper is highly toxic in excess, and results in cellular damage and hepatocellular carcinomas (HCC). This study addresses changes in expression of copper-related genes and metal accumulation in hyperplastic liver and tumors induced by PP. Male rats were fed diets containing DEHP or clofibrate (CLF) for 3-60 days (hyperplasia) and 4-chloro-6-(2,3 xylidino)-2-pyrimidinyl-thio(N-beta-hydroxyethyl) acetamide for 10 months (HCC). During hyperplasia, an immediate and progressive decrease in serum CP activity was observed (P < 0.05), as were reductions in mRNA levels for both CP and Wilson's disease gene (WD gene, a P-type ATPase) (P < 0.05). Tumor-bearing rats had lower serum CP activity (P < 0.05), and CP and WD gene mRNA levels were reduced in tumors (P < 0.05), and in liver surrounding tumors (SL) (P < 0.05). Metallothionein mRNA showed no consistent changes during hyperplasia. Tumors showed a 2.5-fold induction of metallothionein mRNA (P < 0.05), and a 1.2-fold increase in SL. Temporal increases in liver copper content occurred during hyperplasia, with increases of 2-fold (DEHP) and 3.3-fold (CLF) at 60 days (P < 0.05). Copper content was 2.2-fold higher in tumors (P < 0.05) and 1.7-fold higher in SL; iron did not increase and zinc decreased temporally. Thus, copper accumulation and changes in copper-related gene expression may be contributing factors in liver neoplasia in PP-treated rats. Loss of CP results in decreased free radical scavenger capacity and thus may enhance oxidative damage induced by PPs.  (+info)

Effects of fibrate compounds on expression of plasminogen activator inhibitor-1 by cultured endothelial cells. (7/224)

The consistent positive correlation between triglyceride and plasminogen activator inhibitor-1 (PAI-1) levels in plasma and the fact that very low density lipoprotein (VLDL) induces secretion of PAI-1 from cultured human umbilical vein endothelial cells (HUVECs) and human hepatoblastoma cells have raised the question of whether fibrate treatment, the main effect of which is a profound lowering of plasma concentrations of VLDL, might improve fibrinolytic function by reducing the plasma levels of PAI-1. However, the findings of controlled clinical trials using various fibrate compounds have been discrepant. ECs express PAI-1 under normal conditions in humans. We therefore examined the effects of several fibrate compounds on PAI-1 expression and secretion by cultured HUVECs and the HUVEC-derived cell line EA.hy926. All fibrate compounds examined had significant effects on PAI-1 gene transcription in the EA.hy926 cells. Low concentrations of clofibric acid and bezafibrate increased PAI-1 transcription and secretion, whereas Wy-14643 increased PAI-1 synthesis in a dose-dependent way. In contrast, both fenofibric acid and gemfibrozil markedly decreased PAI-1 transcription and secretion from HUVECs and EA.hy926 cells. Thus, stimulation of the transcriptional activity of the PAI-1 gene by some fibrates is linked to increased secretion of PAI-1 protein by the cells, whereas the opposite effects occur with other fibrate compounds. Whether the different effects on PAI-1 transcription and secretion by ECs in vitro also reflect differences in treatment effects on the regulation of plasma PAI-1 activity in vivo will have to be determined in larger-scale, controlled clinical trials.  (+info)

Dual role for Hsc70 in the biogenesis and regulation of the heme-regulated kinase of the alpha subunit of eukaryotic translation initiation factor 2. (8/224)

The heme-regulated kinase of the alpha subunit of eukaryotic initiation factor 2 (HRI) is activated in rabbit reticulocyte lysate (RRL) in response to a number of environmental conditions, including heme deficiency, heat shock, and oxidative stress. Activation of HRI causes an arrest of initiation of protein synthesis. Recently, we have demonstrated that the heat shock cognate protein Hsc70 negatively modulates the activation of HRI in RRL in response to these environmental conditions. Hsc70 is also known to be a critical component of the Hsp90 chaperone machinery in RRL, which plays an obligatory role for HRI to acquire and maintain a conformation that is competent to activate. Using de novo-synthesized HRI in synchronized pulse-chase translations, we have examined the role of Hsc70 in the regulation of HRI biogenesis and activation. Like Hsp90, Hsc70 interacted with nascent HRI and HRI that was matured to a state which was competent to undergo stimulus-induced activation (mature-competent HRI). Interaction of HRI with Hsc70 was required for the transformation of HRI, as the Hsc70 antagonist clofibric acid inhibited the folding of HRI into a mature-competent conformation. Unlike Hsp90, Hsc70 also interacted with transformed HRI. Clofibric acid disrupted the interaction of Hsc70 with transformed HRI that had been matured and transformed in the absence of the drug. Disruption of Hsc70 interaction with transformed HRI in heme-deficient RRL resulted in its hyperactivation. Furthermore, activation of HRI in response to heat shock or denatured proteins also resulted in a similar blockage of Hsc70 interaction with transformed HRI. These results indicate that Hsc70 is required for the folding and transformation of HRI into an active kinase but is subsequently required to negatively attenuate the activation of transformed HRI.  (+info)

Pharmaceuticals in the aquatic environment is an emerging issue and the risks they pose are mostly unknown. They are used in large amounts throughout the world and can enter the environment, as the active metabolite or unmetabolised, through excretion by people and improper disposal. As these drugs are designed to have specific biological effects in a specific organism (as well as sometimes having other non-specific side effects), their potential to cause effects within the environment is great. Clofibric acid (the major metabolite of the lipid lowering drug, Clofibrate) is non-biodegradable, highly motile, very persistent and frequently detected at μg/I levels in the environment. I studied possible effects of clofibric acid in fish, using different experimental approaches and endpoints. The studies involve two different species, and for one of these species, fish at different stages of development. The chapters within this thesis have presented the first evidence (albeit preliminary) of ...
Clofibric Acid, A Peroxisome Proliferator-Activated Receptor Alpha Agonist, forms a Ternary Complex with the Ferric Iron, Yahia Z Hamada, Samid Rehan,
The degradation of an aqueous solution of clofibric acid was investigated during catalytic and non-catalytic ozonation. The catalyst, TiO(2), enhanced the production of hydroxyl radicals from ozone and raised the fraction or clofibric acid degraded b
Micronized CCI-779 is described. This directly compressible rapamycin 42-ester with 3-hydroxy-2-(hydroxymethyl)-2-methylpropionic acid provides a convenient and effective method to deliver therapeutic
Aqueous Solutions NMR, UV-Vis and Potentiometric Titrations of Cd2+ and Hg2+ with Clofibric Acid, Yahia Z Hamada, Khadijah Darboe, Aisha Darboe
TY - JOUR. T1 - Differences in cell proliferation in rodent and human hepatic derived cell lines exposed to ciprofibrate. AU - Clemencet, Marie Claude. AU - Muzio, Giuliana. AU - Trombetta, Antonella. AU - Peters, Jeffrey M.. AU - Gonzalez, Frank J.. AU - Canuto, Rosa A.. AU - Latruffe, Norbert. PY - 2005/5/26. Y1 - 2005/5/26. N2 - Humans appear to be refractory to some effects of peroxisome proliferators including alterations in cell proliferation, whereas rodents are susceptible. In this study, differences between the human and rat response to peroxisome proliferators were evaluated using rat and human tumour liver cell lines. Rat 7777 cells were more responsive than human HepG2 cells to ciprofibrate as they exhibited a higher decrease in cell number than HepG2, and underwent apoptosis. Results from these studies reveal a surprising response in tumour cell lines as the typical in vivo response of increased cell proliferation and reduced apoptosis was not observed in rat tumour cell lines at ...
Inductions of FABP in hepatic cytosol by administration of tiadenol and clofibric acid were studied in rats, mice and guinea-pigs. In rats and mice, [1-14C]oleic acid-binding capacity of hepatic cytosol was increased, in association with induction of
Linking of different ethnicities, races and religions to lipid profile patterns and hypolipidaemic drug usage patterns in coronary artery disease patients
Our study demonstrates that the antihyperlipidemic clofibrate derivatives, which are structurally different from the known activator, sulfobromophthalein, exert stimulatory effects specifically on AKR 1C4 of human liver 3αHSD isoforms. For the activation by sulfobromophthalein, there has been no direct information about the structurally specific interaction between the molecule and the enzyme, except for its sulfonyl group(s) (Matsuura et al., 1996,1997). Our results of the comparative study of the efficacy of the antihyperlipidemic drugs and their related compounds provide the following specific structural requisites for the activator. 1) The existence of a negatively charged carboxyl group, together with at least a hydrophobic aromatic ring, in the activator molecule is necessary to interact with the activator site of the enzyme, because the clofibric acid derivatives lacking the free carboxyl group or the aromatic ring did not activate. Because the pKa values of the carboxyl group of the ...
This page contains information on the chemical Acetic acid, (p-chlorophenoxy)-, 2-isopropylhydrazide including: 18 synonyms/identifiers.
34812-33-4 - OOTGVNOBTIPORR-UHFFFAOYSA-N - Acetic acid, 2-(p-chlorophenoxy)-, 2-(hexahydro-1,4-oxazepin-4-yl)ethyl ester - Similar structures search, synonyms, formulas, resource links, and other chemical information.
In that it can lead cialis compare prices to several times with non-coring 70 huber central venous catheter. Deca- proteins, with an after-treatment of the piping must be cautious in concluding no inter- action studies including zidovudine, lamivudine, aciclovir, ciprofloxacin, tenofo- vir disoproxil fumarate (stribild), plasma trough concentrations of diphtheria toxin fragments a and prolongs blood-clotting time. Eur j hosp pharm 19:243 17. Since the buttery can- 16 % solution. 1.1). The highlighted 12 such studies and are associated with community drug team, has been of some specications may be considered in very strong inhibitor hy- pralidoxime chloride is required. Multiple probe substrates was devel- oped countries, and diabetes mellitus 201 table 13.4 proportion of individuals 1 year rapidly to 2-p-chlorophenoxy-2-methylpropionic acid ho eslerases in vivo [39]. In contrast, if the patient soluble tablet tablet to be aware of the active substance is inuenced by electrolytes or wetting of ...
The hepatic transport of organic anions has been studied extensively. In rats, sinusoidal uptake of many organic anions is mediated by the oatp proteins (oatp1 and oatp2) whose substrates include bile acids as well as nonbile acid organic anions (Meier et al., 1997; Muller and Jansen, 1998). Additionally, at least three other carrier systems may mediate sinusoidal uptake of nonbile acid organic anions, including another family of multispecific transporters (oat) (Sekine et al., 1998), bilitranslocase and bromosulfophthalein/bilirubin-binding protein (Meier et al., 1997). Sinusoidal efflux of organic anions from the liver also has been shown to be carrier-mediated (De Vries et al., 1985; Evans et al., 1995). In this study, the appearance in perfusate of acetaminophen glucuronide and clofibric acid glucuronide during perfusions with the respective parent aglycones (Fig. 1) demonstrates sinusoidal efflux of hepatically generated ether and acyl glucuronides. Although the identity of the efflux ...
See Contraindications. ALT elevations with HCV regimen ombitasvir/paritaprevir/ritonavir, with or without dasabuvir; discontinue Portia prior to starting HCV regimen and restart 2wks after completion. May be antagonized by phenytoin, barbiturates, carbamazepine, bosentan, felbamate, griseofulvin, oxcarbazepine, rifampicin, topiramate, rifabutin, rufinamide, aprepitant, St. Johns wort; use backup contraception. May be potentiated by atorvastatin, rosuvastatin, acetaminophen, ascorbic acid, or CYP3A4 inhibitors (eg, itraconazole, ketoconazole, voriconazole, fluconazole, grapefruit juice). May be affected by HIV protease inhibitors. Concomitant colesevelam; give 4hrs apart. May antagonize acetaminophen, temazepam, salicylic acid, morphine, clofibric acid, lamotrigine. May potentiate cyclosporine, prednisolone, theophylline, tizanidine, voriconazole. May need dose adjustment of thyroid hormones. May affect lab tests (eg, coagulation factors, triglycerides, lipids, glucose tolerance, binding ...
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Reactivity: Human - Sample Type: Cell Culture Supernatant, Plasma. | Order Peroxisome Proliferators Activator beta ELISA Kit (ABIN771143).
Salmon oil is known for being exceptionally rich in omega-3 fats, which are linked to a variety of health benefits. This article lists 8 impressive benefits of salmon oil.
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See Contraindications. ALT elevations with HCV regimen ombitasvir/paritaprevir/ritonavir, with or without dasabuvir; discontinue Tri-Sprintec prior to starting HCV regimen and restart 2wks after completion. May be antagonized by phenytoin, barbiturates, carbamazepine, bosentan, felbamate, griseofulvin, oxcarbazepine, rifampicin, topiramate, rifabutin, rufinamide, aprepitant, St. Johns wort; use backup contraception. May be potentiated by atorvastatin, rosuvastatin, acetaminophen, ascorbic acid, or CYP3A4 inhibitors (eg, itraconazole, ketoconazole, voriconazole, fluconazole, grapefruit juice). May be affected by HIV protease inhibitors. Concomitant colesevelam; give 4hrs apart. May antagonize acetaminophen, temazepam, salicylic acid, morphine, clofibric acid, lamotrigine. May potentiate cyclosporine, prednisolone, theophylline, tizanidine, voriconazole. May need dose adjustment of thyroid hormones. May affect lab tests (eg, coagulation factors, triglycerides, lipids, glucose tolerance, binding ...
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Electrokinetic supercharging-electrospray ionisation-mass spectrometry for separation and on-line preconcentration of hypolipidaemic drugs in water samples
The benefits of salmon oil are numerous and, in general, side effects are rare. Salmon oil has proven to be excellent and extremely important for health.
Salmon Oil for dogs, is extremely beneficial. It is full of Omega 3 fatty acids and vitamins, but what are the benefits, the dosage and where can you buy it?
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Stinky stinky stinky!! We had a speaker at the cavalier club advise salmon oil for an EFA. I bought some from sitstay and put it on the food tonight. The dogs loved it but, man, Jakes breath stinks big time!! Cathy
Little is known about the relationships between hyperlipidemia and bile acid metabolism. However, hypolipidemic treatment with fibric acid derivatives has been shown to increase biliary cholesterol secretion, presumably by reducing bile acid synthesis. To clarify such relationships, we investigated the effects of different hyperlipoproteinemic conditions and of treatment with fibric acid derivatives on the rates of cholesterol 7 alpha-hydroxylation (the limiting step of bile acid synthesis) in humans. We studied 10 patients (aged 36 to 68 years) with lipoprotein phenotype IIa and with a clinical diagnosis of heterozygous familial hypercholesterolemia, a condition of reduced activity of LDL receptors, and 11 patients (aged 48 to 70 years) with lipoprotein phenotype IIb or IV and clinical diagnosis of familial combined hyperlipidemia, a condition probably related to increased hepatic lipoprotein synthesis. Cholesterol 7 alpha-hydroxylation rates were assayed in vivo by tritium release assay after ...
TY - JOUR. T1 - A protein histidine kinase induced m rat liver by peroxisome proliferators. In vitro activation by Ras protein and guanine nucleotides. AU - Motojima, Kiyoto. AU - Goto, S.. PY - 1993/3/15. Y1 - 1993/3/15. N2 - A novel protein kinase is induced in rat liver plasma membrane by the administration of peroxisome proliferators. A 36 kDa protein (P36) on the membrane was rapidly phosphorylated in vitro by the kinase and the phosphorylated amino acid was identified as phosphohistidine. Histidine phosphorylation of P36 was activated in vitro by recombinant Ras protein and GTP; both decreased Michaelis constant (Km) for ATP from 1.25 to 0.25 μM. The novel histidine kinase, products of which have been overlooked due to their acid lability, may participate in cellular signaling and peroxisome proliferators may perturb the pathway.. AB - A novel protein kinase is induced in rat liver plasma membrane by the administration of peroxisome proliferators. A 36 kDa protein (P36) on the membrane ...
Peroxisome proliferators are a diverse group of chemicals, including several hypolipidaemic drugs, that activate a nuclear hormone receptor termed the peroxisome proliferator activated receptor (PPAR). The peroxisomal enzyme acyl CoA oxidase (ACO) is the most widely used marker of peroxisome prolife …
PEROXISOME PROLIFERATION DINP is in a class of chemicals known as peroxisome proliferators - chemicals that induce an increase in the size and number of a subcellular organelle known as a peroxisome in the liver cells of rodents. Many peroxisome proliferators are known to cause liver tumors in rodents. As observed with peroxisome proliferators, including DINP, rats and mice are susceptible to the morphological, biochemical, and carcinogenic effects of peroxisome proliferators, while non-human primates and humans are completely non-responsive or refractory. Criteria have been established by IARC to make the determination that tumors resultant from peroxisomal proliferation are not relevant to humans (IARC, 1995 at 12-13): (a) Information is available to exclude mechanisms of carcinogenesis other than those related to peroxisome proliferation. (b) Peroxisome proliferation (increases in peroxisome volume density or fatty acid b-oxidation activity) and hepatocellular proliferation have been ...
Singh, Kavita, Ramesh Chander and Narinder K. Kapoor (1997) Guggulsterone, a potent hypolipidaemic, prevents oxidation of low density lipoprotein. [Publication] Full text not available from this repository ...
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Crosstalk between the thyroid hormone and peroxisome proliferator-activated receptors in regulating peroxisome proliferator-responsive genes.: Peroxisome prolif
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You may not want to go thru this lol---but I skinned the mice and pulled intestines out. I also cut them up in pieces and put salmon oil on them as you mentioned. As they started eating them, I did leave fur on them and still cut them up and patted with salmon oil ...
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Tricor is prescribed medicine to treat high cholesterol and high triglyceride levels. This medicine is also called as Fenofibrate. Tricor is connected with the set of drugs called fibric acid derivatives or cholesterol reducing drugs.
Tricor is prescribed medicine to treat high cholesterol and high triglyceride levels. This medicine is also called as Fenofibrate. Tricor is connected with the set of drugs called fibric acid derivatives or cholesterol reducing drugs.
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Efficacy and tolerance of 1-(theophyllin-7-yl)-ethyl-2-[2-(p-chlorophenoxy)-2-methylpropionate] (etofylline clofibrate, Duolip… Expand ...
Bezafibrate(Abeita) generic is a fibrate drug, prescribed for high cholesterol in blood. It works mainly by stimulating the action of two enzymes.
Bezalip SR: Bezafibrate belongs to the class of medications known as fibrates. Bezafibrate is used in addition to diet and other measures to treat high cholesterol. It is especially useful in reducing triglycerides, a type of lipid (fat).
Since their discovery in the early 1990s, the peroxisome proliferator activated receptors (PPARs) have attracted significant attention. This is…
Clofibric acid Phenoxy herbicides Merck Index, 11th Edition, 5666. Record of Mecoprop in the GESTIS Substance Database of the ... Mecoprop (also known as methylchlorophenoxypropionic acid and MCPP) is a common general use herbicide found in many household ... propionic acid (mecoprop)". Acta Crystallogr. B. 36 (4): 992-994. doi:10.1107/S0567740880005134. Mecoprop Pesticide Information ...
... clofibric acid), which is the true hypolipidemic agent. So clofibride, just like clofibrate is a prodrug of clofibric acid. ... In the body it is converted into 4-chlorophenoxyisobutyric acid ( ...
It is a combined ester of clofibric acid and niacin (nicotinic acid) with 1,3-propanediol. In the body, the ester is split to 1 ... 3-propanediol and both acids which work in the same way, lowering lipids in blood. v t e. ...
Studies in 1975 and 1977 found clofibric acid and salicylic acids at trace concentrations in treated water. Widespread concern ... Pharmaceutical residues that have been conjugated (bound to a bile acid) before being excreted from the patients may undergo de ... the most toxic effect is due to the combustion of polyvinyl chloride since it produces hydrochloric acid (HCl) which is an ... separation of Al and Polymers using the hydrometallurgical method which uses hydrochloric acid (HCl) can be incorporated. Then ...
... is a fibrate that has been used for the treatment of hyperlipidemia.The substance is a double ester of clofibric acid with 1,3- ... propanediol which is cleaved in the body to one molecule of 1,3-propanediol and two molecules of clofibric acid which is the ...
The molecular formula C10H11ClO3 (molar mass: 214.64 g/mol, exact mass: 214.0397 u) may refer to: Clofibric acid Mecoprop This ...
... clofibric acid (INN) clofibride (INN) clofilium phosphate (INN) clofluperol (INN) clofoctol (INN) cloforex (INN) clofurac (INN ... clodronic acid (INN) clofarabine (USAN) clofazimine (INN) clofedanol (INN) clofenamic acid (INN) clofenamide (INN) clofenciclan ... clavulanic acid (INN) Clavulin (GlaxoSmithKline) clazolam (INN) clazolimine (INN) clazuril (INN) Clear Away Disc Clear By ... clorindanic acid (INN) clorindanol (INN) clorindione (INN) clormecaine (INN) clorofene (INN) cloroperone (INN) cloroqualone ( ...
Chlorophacinone Chlorpyrifos Chloropicrin Chlorothalonil Chlortoluron Chromated copper arsenate Cinnamaldehyde Clofibric acid ... 5-Trichlorophenoxyacetic acid Triclopyr Trifluralin Triazofos Trophobiosis Ultra-low volume Uragan D2 UK Pesticides Campaign ... 4-Dichlorophenoxyacetic acid 1,3-Dichloropropene Dichlorprop Dichlorvos Dicrotophos 1,3-Difluoro-2-propanol Dimethenamid ... Cyhalothrin Cyromazine Davicil DCMU DDT DDT in Australia DDT in New Zealand DDT in the United States Dehydroacetic acid ...
Some derivatives of clofibric acid are in a drug class called fibrates. Phenoxy herbicides to which the compound is chemically ... Clofibric acid is a biologically active metabolite of the lipid-lowering drugs clofibrate, etofibrate and theofibrate with the ... Buser, Hans-Rudolf; Müller, Markus D; Theobald, Norbert (1998). "Occurrence of the Pharmaceutical Drug Clofibric Acid and the ... "Biodegradation of clofibric acid and identification of its metabolites". Journal of Hazardous Materials. 241-242: 182-189. doi: ...
Some derivatives of clofibric acid are in a drug class called fibrates. Phenoxy herbicides to which the compound is chemically ... Clofibric acid is a biologically active metabolite of the lipid-lowering drugs clofibrate, etofibrate and theofibrate with the ... Buser, Hans-Rudolf; Müller, Markus D; Theobald, Norbert (1998). "Occurrence of the Pharmaceutical Drug Clofibric Acid and the ... "Biodegradation of clofibric acid and identification of its metabolites". Journal of Hazardous Materials. 241-242: 182-189. doi: ...
Chlorofibrinic acid; Chlorophibrinic acid; Clofibrate free acid; Clofibrin; Clofibrinic acid; CPIB; Propionic acid, 2-(p- ... methylpropionic acid; «alpha»-(4-Chlorophenoxy)isobutyric acid; (p-Chlorophenoxy)isobutyric acid; Acetic acid, (p-chlorophenoxy ... isobutyric acid; «alpha»-(p-Chlorophenoxy)isobutyric acid; Propanoic acid, 2-(4-chlorophenoxy)-2-methyl-; «alpha»-(4- ... isobutyric acid; 4-CPIB; Acide (p-chlorophenoxy)-2 methyl-2 propionique; Clofibrinsaeure; Propanoic acid, 2-methyl, 2-(4- ...
a zip file of the full study records in XML for all studies in the search results table (max 10000 ...
The catalyst, TiO(2), enhanced the production of hydroxyl radicals from ozone and raised the fraction or clofibric acid ... The degradation of an aqueous solution of clofibric acid was investigated during catalytic and non-catalytic ozonation. ... Clofibric Acid / chemistry*. Ecotoxicology / methods*. Hydrocarbons, Aromatic / analysis, chemistry. Hydroxyl Radical / ... The rate constant for the reaction of clofibric acid and hydroxyl radicals was not affected by the presence of the catalyst. ...
Clofibric acid is metabolized to an acyl glucuronide, clofibric acid glucuronide, which is extensively excreted into bile. The ... Approximately 1.6% of the dose was recovered as clofibric acid in bile and may have been due to hydrolysis of clofibric acid ... For binding interaction studies, either clofibric acid (200 μM), clofibric acid glucuronide (15 μM), acetaminophen (200 μM), or ... Clofibric acid and clofibric acid glucuronide were measured by HPLC based on a method for GG (Sallustio and Fairchild, 1995) ...
... of clofibric acid having effects on both adult and embryo fish. When fathead minnow embryos were exposed to clofibric acid, the ... Clofibric acid (the major metabolite of the lipid lowering drug, Clofibrate) is non-biodegradable, highly motile, very ... The results from this research show that there are effects of clofibric acid in pathways which were not only unexpected in fish ... These effects indicate that clofibric acid may potentially have an impact on fish fecundity, and even more worryingly, on human ...
UV-Vis and Potentiometric Titrations of Cd2+ and Hg2+ with Clofibric Acid, Yahia Z Hamada, Khadijah Darboe, Aisha Darboe ... Figure 2:Potentiometric titration of Cd2+ and Clofibric Acid (CA) in 1:1 molar ratio. Cd2+ Concentration is 2.0 Ã Â 10-3 M in ... Figure 2 shows the potentiometric titration plots of Cd2+ and Clofibric Acid (CA) in 1:1 molar ratio. Cd2+ concentration is 2.0 ... Aqueous Solutions NMR, UV-Vis and Potentiometric Titrations of Cd2+ and Hg2+ with Clofibric Acid. Yahia Z Hamada*, Khadijah ...
Clofibric Acid, A Peroxisome Proliferator-Activated Receptor Alpha Agonist, forms a Ternary Complex with the Ferric Iron, ... was optimized for detection of clofibric acid and its analog ferric clofibric acid. Mass spectrometry data of each compound was ... Scheme 1: Structural formula of clofibric acid (CA), or [2-(4-chlorophenoxy)-2-methylpropanoic acid] (Chemical formula C10H11 ... Clofibric Acid, A Peroxisome Proliferator-Activated Receptor Alpha Agonist, forms a Ternary Complex with the Ferric Iron. Yahia ...
Clofibric acid and gemfibrozil removal in membrane bioreactors The removal of two blood lipid regulators, clofibric acid (CLA) ...
... clofibric acid; cyclosporine (Gengraf, Neoral, Sandimmune); medications for HIV or AIDS such as atazanavir (Reyataz), darunavir ... ascorbic acid (vitamin C); atorvastatin (Lipitor); barbiturates; boceprevir (Victrelis; no longer available in U.S.); bosentan ...
Clofibric Acid. Anticholesteremic Agents. Hypolipidemic Agents. Antimetabolites. Molecular Mechanisms of Pharmacological Action ...
Xing Xian Yu, XY, Odle, J & Drackley, JK 2001, Differential induction of peroxisomal β-oxidation enzymes by clofibric acid and ... Differential induction of peroxisomal β-oxidation enzymes by clofibric acid and aspirin in piglet tissues. / Xing Xian Yu, Xian ... Differential induction of peroxisomal β-oxidation enzymes by clofibric acid and aspirin in piglet tissues. American Journal of ... Fingerprint Dive into the research topics of Differential induction of peroxisomal β-oxidation enzymes by clofibric acid and ...
... clofibric acid, DEHP, WY14,643, nafenopin, and LY171883) on the abundances of a large number of proteins in the livers of ... We have investigated the effects of five peroxisome proliferators (PPs : clofibric acid, DEHP, WY14,643, nafenopin, and ...
Clofibric acid. Abstract. Biological advanced oxidation of the pharmaceuticals clofibric acid (CA), carbamazepine (CBZP), ... Oxidation of atenolol, propranolol, carbamazepine and clofibric acid by a biological Fenton-like system mediated by the white- ... Oxidation of atenolol, propranolol, carbamazepine and clofibric acid by a biological Fenton-like system mediated by the white- ...
Clofibric Acid. 882-09-7. CP 775146. 702680-17-9. Fenofibrate. 49562-28-9. ... 468 amino acids. Molecular mass:. 52225 Da. Quaternary structure:. *Heterodimer; with RXRA. This heterodimerization is required ... WY-14643 (Pirinixic Acid). PPARα agonist,selective and highly potent. 50892-23-4. ... Regulates the peroxisomal beta-oxidation pathway of fatty acids. Functions as transcription activator for the ACOX1 and P450 ...
Previous research has shown that several carboxylic acid drugs are genotoxic in isolated mouse hepatocytes, and that DNA damage ... Glucuronidation of carboxylic-acid-containing drugs can yield reactive acyl (ester-linked) glucuronide metabolites that are ... or 2 mM desferrioxamine mesylate prior to co-incubation with 1 mM clofibric acid for 18 h. Compared to vehicle, clofibric acid ... HEK293 cells were incubated for 18 h with vehicle (2.5 mM NaOH), 0.1-2.5 mM clofibric acid or 0.1-1.0 mM benoxaprofen, ...
Y. Yokoyama, B. Xin, T. Shigeto et al., "Clofibric acid, a peroxisome proliferator-activated receptor a. ligand, inhibits ... including fatty and phytanic acids [4], as well as the fibric acid derivatives used in medicine for the treatment of ... and catalyze the oxidation of arachidonic acid to four regioisomeric epoxyeicosatrienoic acids (EETs) [42, 43]. EETs have been ... Furthermore, several fibric acid derivatives bind to and activate human PPARα with limited or no documented unwanted ...
Y. Yokoyama, B. Xin, T. Shigeto et al., "Clofibric acid, a peroxisome proliferator-activated receptor α. ligand, inhibits ... PGE2 enhances angiogenesis through the induction of VEGF [109]. Clofibric acid is a peroxysome proliferator-activated receptor ... 5, 6-dimethyl-xanthenone-4 acetic acid (DMXAA) is a flavonoid causing DNA damage to endothelial cells that induces apoptosis in ...
... acetic acid); nafenopin (2-methyl-2[p-(1,2,3,4-tetrahydro-1-naphthyl)phenoxy]propionic acid); clofibric acid [2-([p]- ... propanoic acid; docosahexaenoic acid; LY171883; linoleic acid; oleic acid; palmitic acid; clofibrate; eicosatetraenoic acid; 8( ... propanoic acid; docosahexaenoic acid; LY171883; oleic acid; palmitic acid; clofibrate; eicosatetraenoic acid; 8(S)-hydroxy-6,8, ... 9-hydroxyoctadecadienoic acid; KRP-297; Iloprost; L783483; petroselinic acid; elaidic acid; erucic acids, linolenic acid; ...
In rats and mice, [1-14C]oleic acid-binding capacity of hepatic cytosol was increased, in association with induction of ... Inductions of FABP in hepatic cytosol by administration of tiadenol and clofibric acid were studied in rats, mice and guinea- ... Clofibric Acid / pharmacology*. Cytosol / enzymology. Fatty Acid-Binding Proteins. Fatty Alcohols / pharmacology*. Guinea Pigs ... Inductions of FABP in hepatic cytosol by administration of tiadenol and clofibric acid were studied in rats, mice and guinea- ...
Clofibric acid derivatives. Studies of drugs other than statins show other drugs can lower the cholesterol, but without ... eicosapentaenoic acid (fish oil)[24]. It is not clear whether to treat to LDL targets. Studies are currently evaluating this.[ ... fenofibrate (fenofibric acid) Fibrates may reduce myocardial infarction, but not mortality according to a meta-analysis.[9] The ... other drugs that have been studied include eicosapentaenoic acid which is a metabolite of fish oil.[24] Ezetimibe, a ...
0 (Hypolipidemic Agents); 23TF67G79M (etofibrate); 48A5M73Z4Q (Atorvastatin Calcium); 53PF01Q249 (Clofibric Acid); AGG2FN16EV ( ... Hydroxylation, loss of methyl propionic acid group, and Crig e mechanism were observed as the oxidation mechanisms of BF ... In the present study, among the 20 patients with PBC treated with ursodeoxycholic acid or bezafibrate, 15 patients were classed ... in the cell culture medium of fibroblasts incubated with palmitic acid for 96h in the presence of 0-800 M BEZ using tandem mass ...
clofibric acid multiple interactions. ISO. RGD:1305741. 6480464. [Diethylnitrosamine co-treated with Clofibric Acid] affects ... valproic acid decreases expression. ISO. RGD:1353043. 6480464. Valproic Acid results in decreased expression of YEATS4 mRNA. ... Diethylnitrosamine co-treated with Clofibric Acid] affects the expression of YEATS4 mRNA. CTD. PMID:17602206. ... all-trans-retinoic acid decreases expression. ISO. RGD:1353043. 6480464. Tretinoin results in decreased expression of YEATS4 ...
... members of which catalyze biotransformation reactions in which lipophilic substrates are conjugated with glucuronic acid to ... clofibric acid multiple interactions. ISO. RGD:69432. 6480464. [Diethylnitrosamine co-treated with Clofibric Acid] affects the ... valproic acid decreases methylation. EXP. 6480464. Valproic Acid results in decreased methylation of UGT2A1 gene. CTD. PMID: ... pirinixic acid decreases expression. ISO. RGD:69432. 6480464. pirinixic acid results in decreased expression of UGT2A1 mRNA. ...
Clofibric acid Phenoxy herbicides Merck Index, 11th Edition, 5666. Record of Mecoprop in the GESTIS Substance Database of the ... Mecoprop (also known as methylchlorophenoxypropionic acid and MCPP) is a common general use herbicide found in many household ... propionic acid (mecoprop)". Acta Crystallogr. B. 36 (4): 992-994. doi:10.1107/S0567740880005134. Mecoprop Pesticide Information ...
New Orleans: 3 (clofibric acid, estrone and naproxen). • Northern New Jersey: 7 (caffeine, carbamazepine, codeine, cotinine, ...
IV MECHANISM OF BLOCK OF MUSCLE TYPE CLC CHANNELS BY CLOFIBRIC ACID DERIVATIVES ...
... acetic acid],2-Azetidinecarboxylic Acid,3,3,3-(Trioxo-1,3,5-triazinetriyl)tri(propionic Acid),3,4-Dimethoxyphthalic Acid, ... butyric Acid,(S)-Piperidine-2-carboxylic Acid,1,1-Ferrocenedicarboxylic Acid,1-Amino-4-bromo-9,10-dioxoanthracene-2-sulfonic ... Cassellas Acid F. [Display Results] Chlorogenic Acid. [Display Results] Clofibric Acid. [Display Results] ... WAND Categories > Chemicals, Organic>Organic Acids >. The WAND Organic Chemicals taxonomy includes the set of substances, ...
Clofibric Acid. Monensin (used on cattle). Carbamazepine. Estrone. Naproxen. Phenytoin. Cotinine. Azithromycin. Roxithromycin. ... The process used to make alkaline water, called electodialysis, divides tap water into alkaline and acid streams. Any acidic ...
  • Clofibric acid (CA) is a Peroxisome proliferator-activated receptorsalpha (PPARα) ligand. (imedpub.com)
  • PPAR γ ligands include long-chain fatty acids, prostaglandins, and other eicosanoids [ 4 ]. (hindawi.com)
  • PPAR δ is ubiquitously expressed and it is most abundant in brain, colon, and skin [ 10 , 11 ], and binds molecules such as fatty acids and prostaglandins [ 4 ]. (hindawi.com)
  • Several compounds bind PPAR α , including fatty and phytanic acids [ 4 ], as well as the fibric acid derivatives used in medicine for the treatment of hyperlipidemias [ 1 ]. (hindawi.com)
  • Although the therapeutic effect of fibrates on lipid metabolism is mediated via nuclear peroxisome proliferator-activated receptor-α (PPAR-α), our results ( 10 ) show that clofibric and bezafibric acids also inhibit TAS1R3 receptors at drug concentrations similar to those needed to activate PPAR-α ( 14 ). (pnas.org)
  • Ciprofibrate and the PPARα agonist Wy14,643 decreased bile acid synthesis in cultured rat hepatocytes and suppressed cholesterol 7α-hydroxylase and sterol 27-hydroxylase activities, paralleled by a similar reduction of the respective mRNAs. (tudelft.nl)
  • A decreased bile acid production by PPARα-mediated downregulation of cholesterol 7α-hydroxylase and sterol 27-hydroxylase may contribute to the increased risk of gallstone formation after fibrate treatment. (tudelft.nl)
  • It was Gustafsson who first identified physiological ligands for a so called "orphan receptor", namely fatty acids for the peroxisome proliferator activated receptor (PPAR), thereby integrating fatty acids into molecular endocrinology. (uh.edu)
  • Activation of peroxisome proliferator-activated receptor-α (PPARα) suppresses postprandial lipidemia through fatty acid oxidation in enterocytes. (semanticscholar.org)
  • PPARα regulates the expression of genes involved in fatty acid β oxidation [2] . (proteopedia.org)
  • PPARδ regulates the expression of genes involved in fatty acid burning in adipose tissue and skeletal muscle [4] . (proteopedia.org)
  • While PPARα is the major regulator of fatty acid oxidation and uptake in the liver, PPARγ is expressed at extremely high levels in adipose tissue, macrophages, and the large intestine, and controls lipid adipogenesis and energy conversion. (proteopedia.org)
  • [11] These nuclear receptors are of critical importance to the body as exemplified by PPARα knockdown mice suffering from a variety of metabolic defects including hypothermia, elevated plasma free fatty acid levels, and hypoglycemia , potentially leading to death. (proteopedia.org)
  • PPARγ binds polyunsaturated fatty acids like linoleic acid, linolenic acid, and eicosapentaenoic acid at affinities that are in line with serum levels found in the blood. (proteopedia.org)
  • PPARα binds a variety of saturated and unsaturated fatty acids including palmitic acid, oleic acid, linoleic acid, and arachidonic acid. (proteopedia.org)
  • The nuclear receptor peroxisome proliferator-activated receptor (PPAR) α is known primarily as a regulator of fatty acid metabolism, energy balance, and inflammation, but evidence suggests a wider role in regulating the biotransformation of drugs and other lipophilic chemicals. (aspetjournals.org)
  • Furthermore, a humanized CYP3A4/3A7 mouse model showed in vivo induction of CYP3A4 mRNA and protein by [4-chloro-6-(2,3-xylidino)-2-pyrimidinylthio]acetic acid (WY14,643) in liver but not in intestine, whereas hepatic occupancy of PBRs by PPAR α was ligand independent. (aspetjournals.org)
  • Fibrates reduce plasma triglyceride and cholesterol levels via the activation of PPARα, which is considered to be the result of induction of fatty acid catabolism in the liver. (pubmedcentralcanada.ca)
  • At the molecular level, fibrates bind to PPARα and increase the expression of genes that involved in fatty acid uptake (fatty acid binding protein, FABP), β-oxidation (acyl-CoA oxidase, ACOX), and ω-oxidation (cytochrome P450) [ 4 - 7 ]. (pubmedcentralcanada.ca)
  • My results strongly suggest that PPAR is inducible by those compounds known to be peroxisome proliferators (clofibrate and the perfluorinated fatty acids, PFDA & PFOA). (surrey.ac.uk)
  • PPAR alpha is activated by free fatty acids including linoleic, arachidonic, and oleic acids. (novusbio.com)
  • PPAR alpha is expressed mainly in skeletal muscle, heart, liver, and kidney and is thought to regulate many genes involved in the beta-oxidation of fatty acids. (novusbio.com)
  • Recent studies have suggested that n-3 fatty acids, abundant in fish oil, protect against high-fat diet-induced insulin resistance through peroxisome proliferator-activated receptor (PPAR)-α activation and a subsequent decrease in intracellular lipid abundance. (diabetesjournals.org)
  • These data support the hypothesis that n-3 fatty acids protect from high-fat diet-induced hepatic insulin resistance in a PPAR-α-and diacylglycerol-dependent manner. (diabetesjournals.org)
  • Hence, the specific molecular events underlying fish oil and n-3 fatty acid action with respect to restoration of insulin sensitivity appear to involve peroxisome proliferator-activated receptor (PPAR)-α. (diabetesjournals.org)
  • The natural PPAR-α ligands DHA and EPA within physiological concentrations bind to PPAR-α and trigger the following: peroxisome proliferation and transcriptional activation of PPAR-α-responsive genes, such as liver fatty acid binding protein, long-chain fatty acyl-CoA synthetase, peroxisomal acyl-CoA oxidase, bifunctional enzyme, 3-ketoacyl-CoA thiolase, and microsomal 4-hydroxylases CYP4A1 and CYP4A6, among others ( 5 , 14 , 16 - 19 ). (diabetesjournals.org)
  • The transcriptional induction of PPAR-α-responsive genes promotes hepatic intracellular fatty acid uptake, the conversion of fatty acids to their respective fatty acyl-CoA derivatives, and their channeling toward mitochondrial/peroxisomal and endosomal β- and ω-oxidation ( 19 ). (diabetesjournals.org)
  • Biological advanced oxidation of the pharmaceuticals clofibric acid (CA), carbamazepine (CBZP), atenolol (ATL) and propranolol (PPL) is reported for the first time. (ufz.de)
  • Overall, MP lamps proved to be more efficient to maximize the bench-scale degradation of the selected group of compounds (ketoprofen, naproxen, carbamazepine, ciprofloxacin, clofibric acid, and iohexol) by both UV photolysis and UV/H(2)O(2) oxidation. (nih.gov)
  • Some derivatives of clofibric acid are in a drug class called fibrates. (wikipedia.org)
  • Clofibrate and fenofibrate acted as weak inhibitors, and the clofibric acid derivatives that lack the chloro group, methyl group on the α-carbon or carboxyl group greatly decreased the stimulatory effects. (aspetjournals.org)
  • Heparin, platelet-aggregation inhibitors such as salicylic acid and its derivatives (e.g. acetylsalicylic acid, para-aminosalicylic acid, diflunisal), phenylbutazone or other pyrazolone derivatives (sulfinpyrazone), and other non-steroidal anti-inflammatory drugs. (medhelp.org)
  • To investigate the effects of peroxisome proliferators on peroxisomal and mitochondrial β-oxidation in piglet tissues, newborn pigs (1-2 days old) were allowed ad libitum access to milk replacer supplemented with 0.5% clofibric acid (CA) or 1% aspirin for 14 days. (illinois.edu)
  • We have investigated the effects of five peroxisome proliferators (PPs : clofibric acid, DEHP, WY14,643, nafenopin, and LY171883) on the abundances of a large number of proteins in the livers of treated mice at 5- and 35-day time points. (nih.gov)
  • Receptor for peroxisome proliferators such as hypolipidemic drugs and fatty acids. (genecards.org)
  • Concomitant increase by peroxisome proliferators of fatty acid-binding protein, peroxisomal beta-oxidation and cytosolic acyl-CoA hydrolase in liver. (biomedsearch.com)
  • In rats and mice, [1-14C]oleic acid-binding capacity of hepatic cytosol was increased, in association with induction of peroxisomal beta-oxidation, by the administration of either the two peroxisome proliferators. (biomedsearch.com)
  • Studies indicate that PPARs are activated by peroxisome proliferators such as clofibric acid, nafenopin, and WY-14,643, as well as by some fatty acids. (novusbio.com)
  • The NSAIDs that we have tested so far include: Naproxen, Clofibric Acid, Diclofenac, and Ibuprofen. (environmental-expert.com)
  • Although ibuprofen [2-(4-isobutylphenyl)-propionic acid] is one of the most widely consumed drugs in the world, little is known regarding its degradation by environmental bacteria. (asm.org)
  • Ibuprofen-induced washed-cell suspensions also metabolized phenylacetic acid and 2-phenylpropionic acid to catechol, while 3- and 4-tolylacetic acids and 2-(4-tolyl)-propionic acid were metabolized to the corresponding methyl catechols before ring cleavage. (asm.org)
  • These data suggest that, in contrast to the widely distributed coenzyme A ligase, homogentisate, or homoprotocatechuate pathway for metabolism of phenylacetic acid and similar compounds, Ibu-2 removes the acidic side chain of ibuprofen and related compounds prior to ring cleavage. (asm.org)
  • Ibuprofen [2-(4-isobutylphenyl)-propionic acid] is a pharmaceutical drug used for its analgesic, antipyretic, and anti-inflammatory properties. (asm.org)
  • We also provide evidence of an apparently novel metabolic pathway for the degradation of ibuprofen and related phenylacetic acids. (asm.org)
  • Clofibric acid is a biologically active metabolite of the lipid-lowering drugs clofibrate, etofibrate and theofibrate with the molecular formula C10H11ClO3. (wikipedia.org)
  • Clofibric acid (the major metabolite of the lipid lowering drug, Clofibrate) is non-biodegradable, highly motile, very persistent and frequently detected at μg/I levels in the environment. (brunel.ac.uk)
  • PPARs are activated by a vast number of compounds including synthetic drugs such as the clofibrate and anti-diabetic thiazoldinediones, polyunsaturated fatty acids, and a number of eicosanoids, including prostaglandins, lipoxygenase products and oxidized low density lipoprotein [ 2 ]. (imedpub.com)
  • These findings along with the fact that high iron status has been implicated in the increased risk of heart disease, and that anemia has been observed in response to treatment with clofibrate, both in humans and experimental animals, have prompted us to investigate if clofibric acid binds to iron (III) and the nature of such interaction Scheme 1 [ 10 ]. (imedpub.com)
  • The NADP + -dependent dehydrogenase activity of a predominant isoenzyme of human liver 3α-hydroxysteroid dehydrogenase was activated by antihyperlipidemic drugs, such as bezafibrate and clinofibrate, and by clofibric acid and fenofibric acid (active metabolites of clofibrate and fenofibrate, respectively). (aspetjournals.org)
  • I studied possible effects of clofibric acid in fish, using different experimental approaches and endpoints. (brunel.ac.uk)
  • Other results suggested, less pronounced effects of clofibric acid on some other parameters. (brunel.ac.uk)
  • The results from this research show that there are effects of clofibric acid in pathways which were not only unexpected in fish (for example, steroidogenesis, spermatogenesis and gene expression), but also at concentrations below those previously shown to have any biological effects on fish. (brunel.ac.uk)
  • U.S. studies have also confirmed the presence of PPCPs, such as naproxen, estrone, and clofibric acid in drinking water. (eponline.com)
  • Hydroxylation, loss of methyl propionic acid group, and Crig e mechanism were observed as the oxidation mechanisms of BF ozonation. (bireme.br)
  • Side chain hydroxylation has been reported ( 13 , 31 ), along with the formation of carboxyhydratropic acid [2-(4-carboxyphenyl)propionic acid] ( 3 , 31 ) and ibuprofenol [2-(4-isobutylphenyl)-propanol] under anaerobic conditions ( 4 ). (asm.org)
  • The neutral pharmaceuticals (the analgetica phenazone and propyphenazone as well as the enti-epilepticum carbamazepin) and several other acid pharmaceuticals (naproxene, diclofenac) have been removed at a low ozone dosage of 5 mg/LO 3 to below their analytic detection limit. (kompetenz-wasser.de)
  • It has a chemical structure that is characterized by the presence of the 2-phenoxy-2- methylpropanoic acid moiety which has the right ring chelating size to chelate large metal ions such as Cd 2+ and Hg 2+ . (imedpub.com)
  • Clofibric acid Phenoxy herbicides Merck Index, 11th Edition, 5666. (wikipedia.org)
  • The increase in [1-14C]oleic acid binding capacity was responsible for the increase in the content of FABP in livers. (biomedsearch.com)
  • Amtul Z, Westaway D, Cechetto DF, Rozmahel RF (2011b) Oleic acid ameliorates amyloidosis in cellular and mouse models of Alzheimer's disease. (springer.com)
  • One of these was oleic acid, a fatty acid that is found in olive oil and other animal and plant oils. (elifesciences.org)
  • Oleic acid interacts with Musashi-1 in a way that changes the shape of the protein. (elifesciences.org)
  • Musashi-1 appears to act as a 'nutrient sensor', turning down the activity of this enzyme in cells when levels of oleic acid are high, and turning up enzyme activity when oleic acid levels are low. (elifesciences.org)
  • Docosahexaenoic acid (DHA) and arachidonic acid (ARA) are important components of neural membrane phospholipids. (springer.com)
  • Astarita G, Jung KM, Berchtold NC, Nguyen VQ, Gillen DL, Head E, Cotman CW, Piomelli D (2010) Deficient liver biosynthesis of docosahexaenoic acid correlates with cognitive impairment in Alzheimer's disease. (springer.com)
  • Marine oils are rich in n-3 PUFAs, such as eicosapentaenoic acid (20:5n-3) and docosahexaenoic acid (22:6n-3). (aacrjournals.org)
  • The potential of fish oil preserving insulin sensitivity is likely mediated via polyunsaturated ω-3 (n-3) fatty acids, such as DHA (docosahexaenoic acid) and EPA (eicosapentaenoic acid). (diabetesjournals.org)
  • HEK293 cells were incubated for 18 h with vehicle (2.5 mM NaOH), 0.1-2.5 mM clofibric acid or 0.1-1.0 mM benoxaprofen, bezafibrate, or probenecid. (nih.gov)
  • The optimal pH of the activation by the drugs was about 7.5, and the concentrations giving maximum stimulation (1.8- to 2.4-fold) were 100, 50, 400 and 50 μM for bezafibrate, clinofibrate, clofibric acid and fenofibric acid, respectively. (aspetjournals.org)
  • Kinetic analysis with respect to NADP + showed that bezafibrate, clinofibrate, clofibric acid and fenofibric acid were nonessential activators showing dissociation constants of 32, 6, 103 and 11 μM, respectively. (aspetjournals.org)
  • On the other hand, the lipid-lowering agents bezafibrate and clofibric acids have been removed at a slightly higher ozone dosage. (kompetenz-wasser.de)
  • 05), suggesting an interaction between GG and hepatically generated clofibric acid glucuronide at the level of hepatic transport. (aspetjournals.org)
  • suggesting that GG and nonbile acid organic anions may share the same hepatic sinusoidal and canalicular transport systems. (aspetjournals.org)
  • Inductions of FABP in hepatic cytosol by administration of tiadenol and clofibric acid were studied in rats, mice and guinea-pigs. (biomedsearch.com)
  • The hypolipidaemic drug and peroxisome proliferator, clofibric acid was found to produce a significant hepatomegaly and to induce rat hepatic cytochrome P4504A isozyme(s) and peroxisomal β-oxidation at both the protein and molecular level. (surrey.ac.uk)
  • Studies have shown that clofibric acid binds to metals such as copper, and reduces copper-induced oxidation reactions [ 3 , 8 ]. (imedpub.com)
  • The fatty acid binds to the N-terminal RNA Recognition Motif (RRM) and induces a conformational change that prevents RNA association. (elifesciences.org)
  • Regulates the peroxisomal beta-oxidation pathway of fatty acids. (genecards.org)
  • There was no essential difference in the inductions of FABP, acyl-CoA hydrolases and peroxisomal beta-oxidation between tiadenol and clofibric acid, despite a marked difference in their chemical structures. (biomedsearch.com)
  • [13] PPAR's ligand selectivity is intermediate between that of the other isotypes and is activated by palmitic acid and a number of eicosanoids. (proteopedia.org)
  • This fatty acid is metabolized into eicosanoids (PGs, LTs, TXs, and LXs) by COX and LOX enzymes. (springer.com)
  • The ligands for PPARs encompass a range of synthetic compounds and endogenous lipids, including various fatty acids and eicosanoids. (biomedcentral.com)
  • In this study, we examined the influence of 200 μM acetaminophen, acetaminophen glucuronide, and clofibric acid on the disposition of GG (3 μM) in the recirculating isolated perfused rat liver preparation. (aspetjournals.org)
  • The evolution of dissolved organic carbon, specific ultraviolet absorption at 254 nm and the concentration of carboxylic acids monitored the degradation process. (biomedsearch.com)
  • Other researchers from Switzerland, Ireland and Spain in one concerted effort published a detailed paper measuring the stability constants of Cd 2+ with the di-carboxylic acids Malate and Succinate [ 9 ]. (imedpub.com)
  • The transformation products were attributed to the oxidation of amines, which resulted in highly oxidized structures with abundance of carboxylic acids, which started from the formation of amine oxide and the scission of the CN bond of the amide group. (jove.com)
  • The degradation of an aqueous solution of clofibric acid was investigated during catalytic and non-catalytic ozonation. (biomedsearch.com)
  • Qi, X. High-Yield Production of Levulinic Acid from Pretreated Cow Dung in Dilute Acid Aqueous Solution. (mdpi.com)
  • The thermally activated persulfate (PS) degradation of carbon tetrachloride (CT) in the presence of formic acid (FA) was investigated. (hep.com.cn)
  • fenofibrate (fenofibric acid) Fibrates may reduce myocardial infarction , but not mortality according to a meta-analysis . (citizendium.org)
  • HN,CA,CB Chemical shift assignments for apo-Rat intestinal fatty acid binding protein, Clofibric acid-Rat intestinal fatty acid binding protein complex, Fenofibric acid-Rat intestinal fatty acid binding protein complex and Tolfenamic acid-Rat intestinal fatty acid binding protein complex. (wisc.edu)
  • Other routes for the metabolism of phenylacetic acids include the well-characterized homoprotocatechuate ( 27 ) and homogentisate pathways ( 29 ), as well as the more recently described coenzyme A-ligase pathway ( 12 ). (asm.org)
  • They are either obtained from the diet or synthesized from their dietary precursors, a-linolenic acid (ALA) and linoleic acid (LA) in liver. (springer.com)
  • N-3 PUFAs, as compared with linoleic acid, also inhibited the growth of these cells in culture. (aacrjournals.org)
  • Basselin M, Chang L, Seemann R, Bell JM, Rapoport SI (2005) Chronic lithium administration to rats selectively modifies 5-HT2A/2C receptor-mediated brain signaling via arachidonic acid. (springer.com)
  • Increased intake of n-3 PUFAs leads to reduced levels of arachidonic acid (20:4n-6) in tissue lipids and, subsequently, to suppressed production of prostanoids derived from arachidonic acid. (aacrjournals.org)
  • COX, PG endoperoxide synthase, catalyzes the conversion of arachidonic acid to PG endoperoxides. (aacrjournals.org)
  • Likewise, amino acids such as monosodium glutamate (MSG) are ligands of the umami TAS1R1+TAS1R3 receptor. (pnas.org)
  • These residues are part of a hydrogen bonding network that interacts with the carboxylate group of fatty acids and other ligands upon binding. (proteopedia.org)
  • This receptor controls fatty acid metabolism and transport, peroxisomal and mitochondrial β -oxidation [ 3 , 4 ]. (hindawi.com)
  • These results suggest that the long-term therapy with the antihyperlipidemic drugs influences the metabolism of steroid hormones, bile acids and several ketone-containing drugs mediated by the enzyme. (aspetjournals.org)
  • Many genes are involved in fatty acid metabolism including oxidative reaction. (pubmedcentralcanada.ca)
  • Barnekow D, Hamburg A, Puvanesarajah V, Guo M (2001) Metabolism of 2,4-dichlorophenoxyacetic acid in laying hens and lactating goats. (springer.com)
  • Fish oil affects extracellular and intracellular lipid metabolism and decreases the systemic abundance of lipid metabolites in part by accelerating fatty acid catabolism in insulin-sensitive tissues ( 4 , 5 , 9 , 11 - 15 ). (diabetesjournals.org)
  • In this study, we investigated the effect of fibrates on bile acid synthesis. (tudelft.nl)
  • The authors concluded that statins and n-3 fatty acids both reduce cardiac and overall mortality, but that fibrates may increase noncardiovascular mortality. (york.ac.uk)
  • The review classified lipid-lowering interventions in the included studies as statins, fibrates, resins, niacin, n-3 fatty acids and dietary interventions. (york.ac.uk)
  • Of these RCTs, 35 assessed statins, 17 assessed fibrates, 8 assessed resins, 2 assessed niacin, 14 assessed n-3 fatty acids and 17 assessed dietary interventions. (york.ac.uk)
  • Meanwhile, another value-added chemical formic acid could be obtained with a yield of ca. 160 g/kg in the process, implying a total production of ca. 500 g/kg yield for LA and formic acid from the pretreated cow dung with the proposed process. (mdpi.com)
  • The name WW or WWP derives from the presence of two signature tryptophan residues that are spaced 20-23 amino acids apart and are present in most WW domains known to date, as well as that of a conserved Pro. (embl.de)
  • First, there may be long-term cumulative effects we haven't identified yet, especially considering how persistent some residues are-clofibric acid, one by-product of a cholesterol drug, can hang around for two-plus decades. (cityweekly.net)
  • E and F ) Assay scheme for the inhibitor screen ( E ) and F-EMSA dose responses with hits identified from the small molecule screens ( E ) and oleic and elaidic acid ( F ). Each gel is one representative experiment of at least three independent experiments. (elifesciences.org)
  • Identification of intermediates and assessment of ecotoxicity in the oxidation products generated during the ozonation of clofibric acid. (biomedsearch.com)
  • Peroxisomal β-oxidation (POX) of fatty acids is important in lipid catabolism and thermogenesis. (illinois.edu)
  • Xing Xian Yu, XY, Odle, J & Drackley, JK 2001, ' Differential induction of peroxisomal β-oxidation enzymes by clofibric acid and aspirin in piglet tissues ', American Journal of Physiology - Regulatory Integrative and Comparative Physiology , vol. 281, no. 5 50-5, pp. (illinois.edu)
  • Finally, Pseudomonas cepacia has been shown to metabolize 2PPA ( 2 ) and tropic acid ( 21 ) (2-phenyl-3-hydroxypropionic acid) via a pathway involving decarboxylation to phenylacetaldehyde, followed by oxidation to phenylacetic acid ( 2 ). (asm.org)
  • Therefore, the specificity of this induction to clofibric acid and rat liver was investigated. (surrey.ac.uk)
  • The catalyst, TiO(2), enhanced the production of hydroxyl radicals from ozone and raised the fraction or clofibric acid degraded by hydroxyl radicals. (biomedsearch.com)
  • The rate constant for the reaction of clofibric acid and hydroxyl radicals was not affected by the presence of the catalyst. (biomedsearch.com)
  • Fibrate treatment causes adverse changes in biliary lipid composition and decreases bile acid excretion, leading to an increased incidence of cholesterol gallstones. (tudelft.nl)
  • The ester or acyl glucuronides, which are formed from compounds possessing a carboxylic acid group, are chemically reactive metabolites due to the susceptibility of the ester linkage to nucleophilic substitution ( Spahn-Langguth and Benet, 1992 ). (aspetjournals.org)
  • Glucuronidation of carboxylic-acid-containing drugs can yield reactive acyl (ester-linked) glucuronide metabolites that are able to modify endogenous macromolecules. (nih.gov)
  • This study demonstrates the substrate-dependent role of human UGTs in the bioactivation of carboxylic acid drugs to genotoxic acyl glucuronide metabolites that are able to damage nuclear DNA via glycation and/or glycoxidation mechanisms. (nih.gov)
  • All neutral and acid pharmaceutical substances and metabolites examined, have been eliminated entirely at a specifically high ozone dosage of 1,2 mg O 3 /mg DOC 0 . (kompetenz-wasser.de)
  • Mecoprop (also known as methylchlorophenoxypropionic acid and MCPP) is a common general use herbicide found in many household weed killers and "weed-and-feed" type lawn fertilizers. (wikipedia.org)
  • Small differences in the primary amino acid sequence of TAS1R receptors among species are responsible for species selectivity toward many sweeteners. (pnas.org)
  • Glucuronidation of carboxylic acid compounds results in the formation of electrophilic acyl glucuronides. (aspetjournals.org)
  • The most similar compounds whose bacterial metabolisms have been described include 4-isopropylbenzoate (cumate), phenylacetic acid, and 2-phenylpropionic acid (2PPA). (asm.org)
  • Since high iron status has been linked to the increased risk of heart disease, and oxidative stress has been implicated in the etiology of atherosclerosis, this study was undertaken to investigate whether prototypic fibrate, clofibric acid (CA) complexes with ferric iron (Fe3+) and determine the nature of the formed iron complexes. (imedpub.com)
  • A high LA yield of 338.9 g/kg was obtained from the pretreated cow dung, which was much higher than that obtained from the crude cow dung (135 g/kg), mainly attributed to the breakage of the lignin fraction in the lignocellulose structure of the cow dung by potassium hydroxide (KOH) pretreatment, and thus enhanced the accessibility of cow dung to the acid sites in the catalytic reaction. (mdpi.com)
  • Recent proposals for revision of the 1998 Directive include limits on haloacetic acids (formed by reaction of chlorine with organic matter) and chlorite and chlorate (breakdown product of disinfection with chlorine dioxide and decomposition product in stored sodium hypochlorite). (fwr.org)
  • The response of these species and tissues to clofibric acid was compared to their response to phenobarbitone. (surrey.ac.uk)
  • Occurrence of perfluorinated organic acids in the North and Baltic Seas. (uni-hamburg.de)
  • Cafestol (20 μg/mL) had no effect on lithocholic acid 6β-hydroxylase mRNA, another enzyme involved in bile acid synthesis. (tudelft.nl)
  • These findings have suggested that this enzyme also acts as prostaglandin oxidoreductase, carbonyl reductase, dihydrodiol dehydrogenase and bile acid-binding protein in the tissue. (aspetjournals.org)
  • Clofibric acid, an in vivo depressor of coumarin 7-hydroxylase, also depressed hepatocyte activities. (aspetjournals.org)
  • Dietary n-3 polyunsaturated fatty acids (PUFAs), as compared with n-6 PUFAs, suppress cellular production of prostaglandins and tumor cell growth both in vitro and in vivo . (aacrjournals.org)