Tìm thấy 12+ kết quả cho từ khóa "drug metabolism"
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CYPs that are especially important for drug metabolism (Table 5-1) include CYP3A4, CYP3A5, CYP2D6, CYP2C9, CYP2C19, CYP1A2, and CYP2E1, and each drug may be a substrate for one or more of these enzymes. "Phase II". metabolism involves conjugation of specific. The enzymes that accomplish phase II reactions include glucuronyl-, acetyl-, sulfo- and methyltransferases. Drug metabolites may exert important pharmacologic activity, as discussed further below..
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Prodrugs are inactive compounds that require metabolism to generate active metabolites that mediate the drug effects. Drug metabolism has also been implicated in bioactivation of procarcinogens and in generation of reactive metabolites that mediate certain adverse drug effects (e.g., acetaminophen hepatotoxicity, discussed below).. Principles of Pharmacodynamics.
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The pathways related to metabolism in the LL group were pentose and glucuronate interconversions (ko00040), drug metabolism-cytochrome P450 (ko00982), starch and sucrose metabolism (ko00500), metabolism of xenobiotics by cytochrome P450 (ko00980), porphyrin and chlorophyll metabolism (ko00860), retinol metabolism (ko00830), glycine, serine and threonine metab- olism (ko00260), steroid hormone biosynthesis (ko00140) and ascorbate and aldarate metabolism (ko00053) (Fig.
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Validation of quantitative LC/MS methods used in the determination of small- molecule drugs and/or their metabolites in biological fluids is of paramount 620 THE ROLE OF LC–MS IN PK AND DRUG METABOLISM.
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If a drug dose is stabilized in the presence of an inducer that is subsequently stopped, major toxicity can occur as clearance returns to preinduction levels and drug concentrations rise. Individuals vary in the extent to which drug metabolism can be induced, likely through genetic mechanisms.. Interactions that inhibit the bioactivation of prodrugs will similarly decrease drug effects. The analgesic effect of codeine depends on its metabolism to morphine via CYP2D6.
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The concept that genetically determined variations in drug metabolism might be associated with variable drug levels, and hence effect, was advanced at the end of the nineteenth century, and the first examples of familial clustering of unusual drug responses due to this mechanism were noted in the mid-twentieth century. Clinically important genetic variants have been described in multiple molecular pathways of drug disposition (Table 5-1).
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Yoshikawa, Usefulness of the hydrogen–deuterium exchange method in the study of drug metabolism using liquid chromatogra- phy–tandem mass spectrometry, J
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The risk of acetaminophen-related hepatic necrosis is increased in patients receiving drugs such as phenobarbital or phenytoin that increase the rate of drug metabolism or ethanol that exhaust. Generation of an immune response to a drug therefore usually requires in vivo activation and covalent linkage to protein, carbohydrate, or nucleic acid.. The antibody may attack the drug when the drug is covalently attached to a cell and thereby destroy the cell.
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For the more common idiosyncratic reaction to modest doses of medical drugs, altered drug metabolism has been invoked as a likely mechanism. the complexity and specificity of the pathways imply multiple susceptibility loci and would provide an explanation for the rarity of idiosyncratic drug reactions.
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The field of pharmacogenomics seeks to identify genes that alter drug metabolism or confer susceptibility to toxic drug reactions. Pharmacogenomics permits individualized drug therapy, resulting in improved treatment outcomes, reduced toxicities, and more cost-effective pharmaceutical care. As noted above, the identification of genes that increase the risk of specific types of neoplasia is rapidly changing the management of many cancers..
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GSTM2 and GSTA3 in LP group also mediated the decreas- ing trend of the pathways of drug metabolism-cytochrome P450 and metabolism of xenobiotics by cytochrome P450.. metabolism, energy production and oxidation resistance Since pathway analysis revealed that DEGs were predom- inantly enriched in the pathways of PPAR signaling pathway, oxidative phosphorylation and glutathione me- tabolism, the DEGs were subjected to deep-level GO clus- tering analysis in relation to lipid metabolism, energy generation
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Altered drug metabolism (e.g., upon co- administration of rifampin and certain immunosuppressive agents) can be managed with careful monitoring of drug levels and appropriate dose adjustment.. Close follow-up of hepatic enzymes is warranted, particularly during treatment with isoniazid, pyrazinamide, and/or rifampin
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Drug metabolism is the chemical alteration of a drug by the body.. metabolism is what the body does to the drug,. Some drugs are chemically altered by the body (metabolized). Metabolites may be metabolized further instead of being excreted from the body. The termination of the drug effect is caused by bio transformation and excretion .all the substance in the circulatory system , including drugs ,metabolites ,and nutrients will pass through the liver..
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Drug metabolism in the liver.. Sex differences in the circadian variation of cytochrome p450 genes and. Nonredundant roles of the mPer1 and mPer2 genes in the mammalian circadian clock
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Depending on the nature of the drug and the treatment goals, people may deliver drugs into the body in different ways. Absorption is the entry of the drug into the general circulation of the body. The route of drug delivery into the body greatly affects the absorption and effects of the drug..
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Interrupt of Trp metabolism/c-Myc loop efficiently suppressed the drugs resistance induced by TDO2, which represented potential target to improve the outcome in drug-resistant prostatic cancer treatment.. Keywords: Tryptophan metabolism, Kynurenine, AhR, C-Myc, Prostatic cancer. Prostatic cancer is the most commonly diagnosed can- cer, with the third leading cause of cancer associated death in males [1].
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Most of the drug is excreted in the feces. however, in normal individuals, 10% to 20% of the drug is excreted in the urine. In patients with liver disease, hepatic uptake and elimination are reduced and a greater fraction of the drug is excreted in the urine.. responsible for much of the pharmacological activity of allopurinol. Serious reactions preclude further use of the drug.. Probenecid inhibits renal secretion of the glucuronides of NSAIDs such as.
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Trans -chalcone activity against Trichophyton rubrum relies on an interplay between. signaling pathways related to cell wall integrity and fatty acid metabolism. The toxicity of trans- chalcone towards T.
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Regulation of drug efflux and metabolism, activation of bypass signaling or prosurvival pathways, epithelial-mesenchymal transition, promotion of DNA damage repair, stem-like characteristic, remodeling of the microenvironment, and drug resistance (Dong et al., 2020)..
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Data is then collected to evaluate three factors: (1) actual abuse of the drug. (2) the clandestine manufacture of the drug. (3) trafficking and diversion of the drug or its precursors from legitimate channels into clandestine operations. Evidence is also accumulated about the scientific data on the physical and chemical properties of the drug. At this phase of the evaluation, medical uses are also evaluated.. Some of the more commonly encountered Schedule I controlled substances.