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[PMID]:29363349
[Au] Autor:Van Donge T; Mian P; Tibboel D; Van Den Anker J; Allegaert K
[Ad] Endereço:a Intensive Care and Department of Paediatric Surgery , Erasmus MC-Sophia Children's Hospital , Rotterdam , The Netherlands.
[Ti] Título:Drug metabolism in early infancy: opioids as an illustration.
[So] Source:Expert Opin Drug Metab Toxicol;14(3):287-301, 2018 Mar.
[Is] ISSN:1744-7607
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Drug dosing in infants frequently depends on body weight as a crude indicator for maturation. Fentanyl (metabolized by Cytochrome P450 3A4) and morphine (glucuronidated by UDP-glucuronosyltransferase-2B7) served as model drugs to provide insight in maturation patterns of these enzymes and provide understanding of the impact of non-maturational factors to optimize dosing in infants. Areas covered: Systematic searches on metabolism and population pharmacokinetic (Pop-PK) models for fentanyl and morphine were performed. Pre- and post-model selection criteria were applied to assess and evaluate the validity of these models. It was observed that maturational changes have been rather well investigated, be it with variability in the maturational function estimates. The same holds true for Pop-PK models, where non-maturational covariates have also been reported (pharmacogenetics, disease state or external influences), although less incorporated in the PK models and with limited knowledge on mechanisms involved. Expert opinion: PK models for fentanyl and morphine are currently available. Consequently, we suggest that researchers should not continue to develop new models, but should investigate whether collected data fit in already existing models and provide additional value concerning the impact of (non)-maturational factors like drug-drug interactions or pharmacogenetics.
[Mh] Termos MeSH primário: Analgésicos Opioides/administração & dosagem
Fentanila/administração & dosagem
Morfina/administração & dosagem
[Mh] Termos MeSH secundário: Fatores Etários
Analgésicos Opioides/farmacocinética
Peso Corporal
Citocromo P-450 CYP3A/metabolismo
Relação Dose-Resposta a Droga
Fentanila/farmacocinética
Glucuronosiltransferase/metabolismo
Seres Humanos
Lactente
Modelos Biológicos
Morfina/farmacocinética
Farmacogenética
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Analgesics, Opioid); 76I7G6D29C (Morphine); EC 1.14.13.67 (CYP3A4 protein, human); EC 1.14.14.1 (Cytochrome P-450 CYP3A); EC 2.4.1.- (UGT2B7 protein, human); EC 2.4.1.17 (Glucuronosyltransferase); UF599785JZ (Fentanyl)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180125
[St] Status:MEDLINE
[do] DOI:10.1080/17425255.2018.1432595


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[PMID]:29203276
[Au] Autor:Lazarska KE; Dekker SJ; Vermeulen NPE; Commandeur JNM
[Ad] Endereço:AIMMS-Division of Molecular Toxicology, Department of Chemistry and Pharmaceutical sciences, Vrije Universiteit, De Boelelaan 1108, 1081 HZ, Amsterdam, The Netherlands.
[Ti] Título:Effect of UGT2B7*2 and CYP2C8*4 polymorphisms on diclofenac metabolism.
[So] Source:Toxicol Lett;284:70-78, 2018 Mar 01.
[Is] ISSN:1879-3169
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The use of diclofenac is associated with rare but severe drug-induced liver injury (DILI) in a very small number of patients. The factors which predispose susceptible patients to hepatotoxicity of diclofenac are still incompletely understood. Formation of protein-reactive metabolites by UDP-glucuronosyl transferases and cytochromes P450 is commonly considered to play an important role, as indicated by the detection of covalent protein adducts and antibodies in the serum of patients suffering from diclofenac-induced liver injury. Since no associations have been found with HLA-alleles, polymorphisms of genes encoding for proteins involved in the disposition of diclofenac may be important. Previous association studies showed that possession of the UGT2B7*2 and CYP2C8*4 alleles is more common in cases of diclofenac-induced DILI. In the present study, the metabolism of diclofenac by UGT2B7*2 and CYP2C8*4 was compared with their corresponding wild-type enzymes. Enzyme kinetic analysis revealed that recombinant UGT2B7*2 showed an almost 6-fold lower intrinsic clearance of diclofenac glucuronidation compared to UGT2B7*1. The mutant CYP2C8*4 showed approximately 35% reduced activity in the 4'-hydroxylation of diclofenac acyl glucuronide. Therefore, a decreased hepatic exposure to diclofenac acyl glucuronide is expected in patients with the UGT2B7*2 genotype. The increased risk for hepatotoxicity, therefore, might be the result from a shift to oxidative bioactivation to cytotoxic quinoneimines.
[Mh] Termos MeSH primário: Anti-Inflamatórios não Esteroides/metabolismo
Citocromo P-450 CYP2C8/genética
Diclofenaco/metabolismo
Glucuronosiltransferase/genética
Polimorfismo Genético
[Mh] Termos MeSH secundário: Animais
Doença Hepática Induzida por Substâncias e Drogas/metabolismo
Escherichia coli/genética
Glucuronídeos/metabolismo
Hidroxilação
Cinética
Mutação
Oxirredução
Proteínas Recombinantes
Células Sf9
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents, Non-Steroidal); 0 (Glucuronides); 0 (Recombinant Proteins); 144O8QL0L1 (Diclofenac); EC 1.14.14.1 (CYP2C8 protein, human); EC 1.14.14.1 (Cytochrome P-450 CYP2C8); EC 2.4.1.- (UGT2B7 protein, human); EC 2.4.1.17 (Glucuronosyltransferase)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171206
[St] Status:MEDLINE


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[PMID]:29188674
[Au] Autor:Ding BF; Shao L; Zhang RS; Liang C; Zhang YR
[Ad] Endereço:College of Life and Environmental Sciences, Shanghai Normal University, Shanghai 200234, China.
[Ti] Título:[Research Progress on Abused Drugs Metabolic in vivo].
[So] Source:Fa Yi Xue Za Zhi;32(4):290-295, 2016 Aug.
[Is] ISSN:1004-5619
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:Under the catalysis of a variety of metabolic enzymes , such as UDP-glucuronyl transferases, cytochrome P450, carboxylesterase, sulfotransferase, butyrylcholinesterase, catechol- -methyl transferase and 6-morphine dehydrogenase, the drugs perform glucuronidation, hydrolysis, oxidation, sulfonation and other reactions, then translate into active or inactive metabolites, which are excreted through urination, bile or the other pathways at last. Different drugs own their different metabolic pathways. This paper introduces the studies about the metabolism of drugs in human and animal in recent years, such as morphine-like drugs, amphetamine, ketamine, cannabis and cocaine, and reviews the research progress about the sites of metabolism, metabolic enzymes, metabolites and physiological activity of those drugs metabolic .
[Mh] Termos MeSH primário: Colinesterases/metabolismo
Sistema Enzimático do Citocromo P-450/metabolismo
Glucuronosiltransferase/metabolismo
Drogas Ilícitas/metabolismo
[Mh] Termos MeSH secundário: Oxirredutases do Álcool/metabolismo
Animais
Carboxilesterase/metabolismo
Catecol O-Metiltransferase/metabolismo
Seres Humanos
Oxirredução
Sulfotransferases/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Street Drugs); 9035-51-2 (Cytochrome P-450 Enzyme System); EC 1.1.- (Alcohol Oxidoreductases); EC 1.1.1.218 (morphine 6-dehydrogenase); EC 2.1.1.6 (Catechol O-Methyltransferase); EC 2.4.1.17 (Glucuronosyltransferase); EC 2.8.2.- (Sulfotransferases); EC 3.1.1.1 (Carboxylesterase); EC 3.1.1.8 (Cholinesterases)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180215
[Lr] Data última revisão:
180215
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171201
[St] Status:MEDLINE
[do] DOI:10.3969/j.issn.1004-5619.2016.04.013


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[PMID]:28882566
[Au] Autor:Habibi M; Mirfakhraie R; Khani M; Rakhshan A; Azargashb E; Pouresmaeili F
[Ad] Endereço:Department of Medical Genetics, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
[Ti] Título:Genetic variations in UGT2B28, UGT2B17, UGT2B15 genes and the risk of prostate cancer: A case-control study.
[So] Source:Gene;634:47-52, 2017 Nov 15.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Glucuronidation is a major pathway for elimination of exogenous and endogenous compounds such as environmental carcinogens and androgens from the body. This biochemical pathway is mediated by enzymes called uridine diphosphoglucuronosyltransferases (UGTs). Null (del/del) genes polymorphisms in UGT2B17, and UGT2B28 and D85Y single-nucleotide polymorphism (SNP) of UGT2B15 have been reported to increase the risk of prostate cancer. The goal of this study was to determine the association of mentioned genetic variants with the risk of prostate cancer. We investigated the copy number variations (CNVs) of UGT2B17 and UGT2B28 loci and the association between rs1902023 polymorphism of UGT2B15 gene in 360 subjects consisted of 120 healthy controls, 120 prostate cancer (PC) patients and 120 benign prostatic hyperplasia (BPH) patients. No association was detected for the mentioned polymorphisms and the risk of PC. However, a significant association was detected between UGT2B17 copy number variation and BPH risk (OR=2.189; 95% CI, 1.303-3.675; p=0.003). Furthermore, we observed that the D85Y polymorphism increases the risk of BPH when analyzed in combination with the copy number variation of UGT2B17 gene (OR=0.135; 95% CI, 0.036-0.512; p=0.003). Our findings suggest that the D85Y polymorphism of UGT2B15 and CNVs in UGT2B28 and UGT2B17 genes is not associated with prostate cancer risk in Iranian patients. To our knowledge, this is the first report that implicates the role of CNV of UGT2B17 gene in BPH.
[Mh] Termos MeSH primário: Variação Genética
Glucuronosiltransferase/genética
Antígenos de Histocompatibilidade Menor/genética
Hiperplasia Prostática/genética
Neoplasias da Próstata/genética
[Mh] Termos MeSH secundário: Idoso
Estudos de Casos e Controles
Variações do Número de Cópias de DNA
Estudos de Associação Genética
Predisposição Genética para Doença
Seres Humanos
Irã (Geográfico)
Masculino
Meia-Idade
Polimorfismo de Nucleotídeo Único
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Minor Histocompatibility Antigens); EC 2.4.1.- (UDP-glucuronosyltransferase, UGT2B28); EC 2.4.1.17 (Glucuronosyltransferase); EC 2.4.1.17 (UDP-glucuronosyltransferase 2B15, human); EC 2.4.1.17 (UGT2B17 protein, human); EC 2.4.1.17 (UGT2B28 protein, human)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171002
[Lr] Data última revisão:
171002
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170909
[St] Status:MEDLINE


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[PMID]:28863216
[Au] Autor:Gesteira TF; Sun M; Coulson-Thomas YM; Yamaguchi Y; Yeh LK; Hascall V; Coulson-Thomas VJ
[Ad] Endereço:Universidade Federal de Sao Paulo, Sao Paulo, Brazil.
[Ti] Título:Hyaluronan Rich Microenvironment in the Limbal Stem Cell Niche Regulates Limbal Stem Cell Differentiation.
[So] Source:Invest Ophthalmol Vis Sci;58(11):4407-4421, 2017 Sep 01.
[Is] ISSN:1552-5783
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Purpose: Limbal epithelial stem cells (LSCs), located in the basal layer of the corneal epithelium in the corneal limbus, are vital for maintaining the corneal epithelium. LSCs have a high capacity of self-renewal with increased potential for error-free proliferation and poor differentiation. To date, limited research has focused on unveiling the composition of the limbal stem cell niche, and, more important, on the role the specific stem cell niche may have in LSC differentiation and function. Our work investigates the composition of the extracellular matrix in the LSC niche and how it regulates LSC differentiation and function. Methods: Hyaluronan (HA) is naturally synthesized by hyaluronan synthases (HASs), and vertebrates have the following three types: HAS1, HAS2, and HAS3. Wild-type and HAS and TSG-6 knockout mice-HAS1-/-;HAS3-/-, HAS2Δ/ΔCorEpi, TSG-6-/--were used to determine the importance of the HA niche in LSC differentiation and specification. Results: Our data demonstrate that the LSC niche is composed of a HA rich extracellular matrix. HAS1-/-;HAS3-/-, HAS2Δ/ΔCorEpi, and TSG-6-/- mice have delayed wound healing and increased inflammation after injury. Interestingly, upon insult the HAS knock-out mice up-regulate HA throughout the cornea through a compensatory mechanism, and in turn this alters LSC and epithelial cell specification. Conclusions: The LSC niche is composed of a specialized HA matrix that differs from that present in the rest of the corneal epithelium, and the disruption of this specific HA matrix within the LSC niche leads to compromised corneal epithelial regeneration. Finally, our findings suggest that HA has a major role in maintaining the LSC phenotype.
[Mh] Termos MeSH primário: Diferenciação Celular/fisiologia
Microambiente Celular/fisiologia
Epitélio Anterior/metabolismo
Ácido Hialurônico/metabolismo
Limbo da Córnea/citologia
Nicho de Células-Tronco/fisiologia
Células-Tronco/metabolismo
[Mh] Termos MeSH secundário: Animais
Queimaduras Químicas/metabolismo
Modelos Animais de Doenças
Queimaduras Oculares/induzido quimicamente
Glucuronosiltransferase/metabolismo
Hialuronan Sintases
Ácido Hialurônico/genética
Imuno-Histoquímica
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Camundongos Transgênicos
Microscopia Confocal
Microscopia Eletrônica de Transmissão
RNA Mensageiro/genética
Reação em Cadeia da Polimerase em Tempo Real
Hidróxido de Sódio
Cicatrização/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (RNA, Messenger); 55X04QC32I (Sodium Hydroxide); 9004-61-9 (Hyaluronic Acid); EC 2.4.1.17 (Glucuronosyltransferase); EC 2.4.1.212 (Hyaluronan Synthases)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170902
[St] Status:MEDLINE
[do] DOI:10.1167/iovs.17-22326


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[PMID]:28817838
[Au] Autor:Lévi F; Karaboué A; Saffroy R; Desterke C; Boige V; Smith D; Hebbar M; Innominato P; Taieb J; Carvalho C; Guimbaud R; Focan C; Bouchahda M; Adam R; Ducreux M; Milano G; Lemoine A
[Ad] Endereço:INSERM, UMRS 935 Team 'Cancer Chronotherapy and Postoperative Liver Function', Campus CNRS, 7 rue Guy Môquet, and UMRS 1193 'Physiopathology and treatment of Liver diseases', Paul Brousse Hospital, 14 avenue Paul-Vaillant-Couturier, 94800 Villejuif, France.
[Ti] Título:Pharmacogenetic determinants of outcomes on triplet hepatic artery infusion and intravenous cetuximab for liver metastases from colorectal cancer (European trial OPTILIV, NCT00852228).
[So] Source:Br J Cancer;117(7):965-973, 2017 Sep 26.
[Is] ISSN:1532-1827
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The hepatic artery infusion (HAI) of irinotecan, oxaliplatin and 5-fluorouracil with intravenous cetuximab achieved outstanding efficacy in previously treated patients with initially unresectable liver metastases from colorectal cancer. This planned study aimed at the identification of pharmacogenetic predictors of outcomes. METHODS: Circulating mononuclear cells were analysed for 207 single-nucleotide polymorphisms (SNPs) from 34 pharmacology genes. Single-nucleotide polymorphisms passing stringent Hardy-Weinberg equilibrium test were tested for their association with outcomes in 52 patients (male/female, 36/16; WHO PS, 0-1). RESULTS: VKORC1 SNPs (rs9923231 and rs9934438) were associated with early and objective responses, and survival. For rs9923231, T/T achieved more early responses than C/T (50% vs 5%, P=0.029) and greatest 4-year survival (46% vs 0%, P=0.006). N-acetyltransferase-2 (rs1041983 and rs1801280) were associated with up to seven-fold more macroscopically complete hepatectomies. Progression-free survival was largest in ABCB1 rs1045642 T/T (P=0.026) and rs2032582 T/T (P=0.035). Associations were found between toxicities and gene variants (P<0.05), including neutropenia with ABCB1 (rs1045642) and SLC0B3 (rs4149117 and rs7311358); and diarrhoea with CYP2C9 (rs1057910), CYP2C19 (rs3758581), UGT1A6 (rs4124874) and SLC22A1 (rs72552763). CONCLUSION: VKORC1, NAT2 and ABCB1 variants predicted for HAI efficacy. Pharmacogenetics could guide the personalisation of liver-targeted medico-surgical therapies.
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/administração & dosagem
Arilamina N-Acetiltransferase/genética
Neoplasias Colorretais/genética
Neoplasias Hepáticas/tratamento farmacológico
Neoplasias Hepáticas/genética
Vitamina K Epóxido Redutases/genética
[Mh] Termos MeSH secundário: Subfamília B de Transportador de Cassetes de Ligação de ATP/genética
Administração Intravenosa
Adulto
Idoso
Protocolos de Quimioterapia Combinada Antineoplásica/efeitos adversos
Camptotecina/administração & dosagem
Camptotecina/análogos & derivados
Proteínas da Membrana Plasmática de Transporte de Catecolaminas/genética
Cetuximab/administração & dosagem
Neoplasias Colorretais/patologia
Citocromo P-450 CYP2C19/genética
Citocromo P-450 CYP2C9/genética
Diarreia/induzido quimicamente
Diarreia/genética
Intervalo Livre de Doença
Feminino
Fluoruracila/administração & dosagem
Glucuronosiltransferase/genética
Hepatectomia
Artéria Hepática
Seres Humanos
Infusões Intra-Arteriais
Neoplasias Hepáticas/secundário
Neoplasias Hepáticas/cirurgia
Masculino
Meia-Idade
Neutropenia/induzido quimicamente
Neutropenia/genética
Compostos Organoplatínicos/administração & dosagem
Farmacogenética
Polimorfismo de Nucleotídeo Único
Taxa de Sobrevida
Resultado do Tratamento
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE II; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ABCB1 protein, human); 0 (ATP Binding Cassette Transporter, Sub-Family B); 0 (Catecholamine Plasma Membrane Transport Proteins); 0 (Organoplatinum Compounds); 0 (Slc22a1 protein, mouse); 04ZR38536J (oxaliplatin); 7673326042 (irinotecan); EC 1.14.13.- (CYP2C9 protein, human); EC 1.14.13.- (Cytochrome P-450 CYP2C9); EC 1.14.14.1 (Cytochrome P-450 CYP2C19); EC 1.17.4.4 (VKORC1 protein, human); EC 1.17.4.4 (Vitamin K Epoxide Reductases); EC 2.3.1.5 (Arylamine N-Acetyltransferase); EC 2.3.1.5 (NAT2 protein, human); EC 2.4.1.- (UDP-glucuronosyltransferase, UGT1A6); EC 2.4.1.17 (Glucuronosyltransferase); PQX0D8J21J (Cetuximab); U3P01618RT (Fluorouracil); XT3Z54Z28A (Camptothecin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170818
[St] Status:MEDLINE
[do] DOI:10.1038/bjc.2017.278


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[PMID]:28771887
[Au] Autor:Migita T; Takayama KI; Urano T; Obinata D; Ikeda K; Soga T; Takahashi S; Inoue S
[Ad] Endereço:Departments of Anti-Aging Medicine and Geriatric Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
[Ti] Título:ACSL3 promotes intratumoral steroidogenesis in prostate cancer cells.
[So] Source:Cancer Sci;108(10):2011-2021, 2017 Oct.
[Is] ISSN:1349-7006
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Long-chain acyl-coenzyme A (CoA) synthetase 3 (ACSL3) is an androgen-responsive gene involved in the generation of fatty acyl-CoA esters. ACSL3 is expressed in both androgen-sensitive and castration-resistant prostate cancer (CRPC). However, its role in prostate cancer remains elusive. We overexpressed ACSL3 in androgen-dependent LNCaP cells and examined the downstream effectors of ACSL3. Furthermore, we examined the role of ACSL3 in the androgen metabolism of prostate cancer. ACSL3 overexpression led to upregulation of several genes such as aldo-keto reductase 1C3 (AKR1C3) involved in steroidogenesis, which utilizes adrenal androgen dehydroepiandrosterone sulfate (DHEAS) as substrate, and downregulated androgen-inactivating enzyme UDP-glucuronosyltransferase 2 (UGT2B). Exposure to DHEAS significantly increased testosterone levels and cell proliferative response in ACSL3-overexpressing cells when compared to that in control cells. A public database showed that ACSL3 level was higher in CRPC than in hormone-sensitive prostate cancer. CRPC cells showed an increased expression of ACSL3 and an expression pattern of AKR1C3 and UGT2B similar to ACSL3-overexpressing cells. DHEAS stimulation significantly promoted the proliferation of CRPC cells when compared to that of LNCaP cells. These findings suggest that ACSL3 contributes to the growth of CRPC through intratumoral steroidogenesis (i.e. promoting androgen synthesis from DHEAS and preventing the catabolism of active androgens).
[Mh] Termos MeSH primário: Coenzima A Ligases/genética
Coenzima A Ligases/metabolismo
Sulfato de Desidroepiandrosterona/farmacologia
Neoplasias de Próstata Resistentes à Castração/metabolismo
Testosterona/metabolismo
[Mh] Termos MeSH secundário: 3-Hidroxiesteroide Desidrogenases/metabolismo
Membro C3 da Família 1 de alfa-Ceto Redutase
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Glucuronosiltransferase/metabolismo
Seres Humanos
Hidroxiprostaglandina Desidrogenases/metabolismo
Lipogênese
Masculino
Neoplasias de Próstata Resistentes à Castração/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
3XMK78S47O (Testosterone); 57B09Q7FJR (Dehydroepiandrosterone Sulfate); EC 1.1.- (3-Hydroxysteroid Dehydrogenases); EC 1.1.1.- (Hydroxyprostaglandin Dehydrogenases); EC 1.1.1.357 (AKR1C3 protein, human); EC 1.1.1.357 (Aldo-Keto Reductase Family 1 Member C3); EC 2.4.1.17 (Glucuronosyltransferase); EC 6.2.1.- (Coenzyme A Ligases); EC 6.2.1.3 (long-chain-fatty-acid-CoA ligase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170804
[St] Status:MEDLINE
[do] DOI:10.1111/cas.13339


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[PMID]:28753904
[Au] Autor:Cao YF; Du Z; Zhu ZT; Sun HZ; Fu ZW; Yang K; Liu YZ; Hu CM; Dong PP; Gonzalez FJ; Fang ZZ
[Ad] Endereço:Key Laboratory of Contraceptives and Devices Research (NPFPC), Shanghai Engineer and Technology Research Center of Reproductive Health Drug and Devices, Shanghai Institute of Planned Parenthood Research, Shanghai, China.
[Ti] Título:Inhibitory effects of fifteen phthalate esters in human cDNA-expressed UDP-glucuronosyltransferase supersomes.
[So] Source:Chemosphere;185:983-990, 2017 Oct.
[Is] ISSN:1879-1298
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Phthalate esters (PAEs) have been extensively used in industry as plasticizers and there remains concerns about their safety. The present study aimed to determine the inhibition of phthalate esters (PAEs) on the activity of the phase II drug-metabolizing enzymes UDP-glucuronosyltransferases (UGTs). In vitro recombinant UGTs-catalyzed glucuronidation of 4-methylumbelliferone was used to investigate the inhibition potentials of PAEs towards various s UGTs. PAEs exhibited no significant inhibition of UGT1A1, UGT1A3, UGT1A8, UGT1A10, UGT2B15, and UGT2B17, and limited inhibition of UGT1A6, UGT1A7 and UGT2B4. However, UGT1A9 was strongly inhibited by PAEs. In silico docking demonstrated a significant contribution of hydrogen bonds and hydrophobic interactions contributing to the inhibition of UGT by PAEs. The K values were 15.5, 52.3, 23.6, 12.2, 5.61, 2.79, 1.07, 22.8, 0.84, 73.7, 4.51, 1.74, 0.58, 6.79, 4.93, 6.73, and 7.23 µM for BBOP-UGT1A6, BBZP-UGT1A6, BBOP-UGT1A7, BBZP-UGT1A7, DiPP-UGT1A9, DiBP-UGT1A9, DCHP-UGT1A9, DBP-UGT1A9, BBZP-UGT1A9, BBOP-UGT1A9, DMEP-UGT1A9, DPP-UGT1A9, DHP-UGT1A9, DiBP-UGT2B4, DBP-UGT2B4, DAP-UGT2B4, and BBZP-UGT2B4, respectively. In conclusion, exposure to PAEs might influence the metabolic elimination of endogenous compounds and xenobiotics through inhibiting UGTs.
[Mh] Termos MeSH primário: DNA Complementar/metabolismo
Glucuronosiltransferase/metabolismo
Ácidos Ftálicos/toxicidade
[Mh] Termos MeSH secundário: Ésteres/metabolismo
Glucuronídeos/metabolismo
Glucuronosiltransferase/genética
Seres Humanos
Inativação Metabólica
Microssomos Hepáticos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Complementary); 0 (Esters); 0 (Glucuronides); 0 (Phthalic Acids); 6O7F7IX66E (phthalic acid); EC 2.4.1.- (UGT1A1 enzyme); EC 2.4.1.- (bilirubin uridine-diphosphoglucuronosyl transferase 1A10); EC 2.4.1.135 (B3GAT2 protein, human); EC 2.4.1.17 (Glucuronosyltransferase); EC 2.4.1.17 (UDP-glucuronosyltransferase 1A9); EC 2.4.1.17 (UDP-glucuronosyltransferase, UGT1A8)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171011
[Lr] Data última revisão:
171011
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170730
[St] Status:MEDLINE


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[PMID]:28663312
[Au] Autor:Court MH; Zhu Z; Masse G; Duan SX; James LP; Harmatz JS; Greenblatt DJ
[Ad] Endereço:Pharmacogenomics Laboratory (M.H.C., Z.Z.), Program in Individualized Medicine (PrIMe), Department of Veterinary Clinical Sciences, College of Veterinary Medicine, Washington State University, Pullman, Washington; Program in Pharmacology and Experimental Therapeutics (G.M., S.X.D., J.S.H., and D.J.G
[Ti] Título:Race, Gender, and Genetic Polymorphism Contribute to Variability in Acetaminophen Pharmacokinetics, Metabolism, and Protein-Adduct Concentrations in Healthy African-American and European-American Volunteers.
[So] Source:J Pharmacol Exp Ther;362(3):431-440, 2017 Sep.
[Is] ISSN:1521-0103
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Over 30 years ago, black Africans from Kenya and Ghana were shown to metabolize acetaminophen faster by glucuronidation and slower by oxidation compared with white Scottish Europeans. The objectives of this study were to determine whether similar differences exist between African-Americans and European-Americans, and to identify genetic polymorphisms that could explain these potential differences. Acetaminophen plasma pharmacokinetics and partial urinary metabolite clearances via glucuronidation, sulfation, and oxidation were determined in healthy African-Americans (18 men, 23 women) and European-Americans (34 men, 20 women) following a 1-g oral dose. There were no differences in acetaminophen total plasma, glucuronidation, or sulfation clearance values between African-Americans and European-Americans. However, median oxidation clearance was 37% lower in African-Americans versus European-Americans (0.57 versus 0.90 ml/min per kilogram; = 0.0001). Although acetaminophen total or metabolite clearance values were not different between genders, shorter plasma half-life values (by 11-14%; < 0.01) were observed for acetaminophen, acetaminophen glucuronide, and acetaminophen sulfate in women versus men. The UGT2B15*2 polymorphism was associated with variant-allele-number proportional reductions in acetaminophen total clearance (by 15-27%; < 0.001) and glucuronidation partial clearance (by 23-48%; < 0.001). UGT2B15 *2/*2 genotype subjects also showed higher acetaminophen protein-adduct concentrations than *1/*2 (by 42%; = 0.003) and *1/*1 (by 41%; = 0.003) individuals. Finally, CYP2E1 *1D/*1D genotype African-Americans had lower oxidation clearance than *1C/*1D (by 42%; = 0.041) and *1C/*1C (by 44%; = 0.048) African-Americans. Consequently, African-Americans oxidize acetaminophen more slowly than European-Americans, which may be partially explained by the CYP2E1*1D polymorphism. UGT2B15*2 influences acetaminophen pharmacokinetics in both African-Americans and European-Americans.
[Mh] Termos MeSH primário: Acetaminofen/análogos & derivados
Acetaminofen/farmacocinética
Afroamericanos/genética
Analgésicos não Entorpecentes/farmacocinética
Cisteína/análogos & derivados
Grupo com Ancestrais do Continente Europeu/genética
Polimorfismo Genético
[Mh] Termos MeSH secundário: Acetaminofen/sangue
Acetaminofen/metabolismo
Acetaminofen/urina
Analgésicos não Entorpecentes/sangue
Analgésicos não Entorpecentes/urina
Cisteína/metabolismo
Feminino
Frequência do Gene
Glucuronídeos/metabolismo
Glucuronosiltransferase/genética
Voluntários Saudáveis
Seres Humanos
Masculino
Taxa de Depuração Metabólica/genética
Desentoxicação Metabólica Fase I/genética
Desintoxicação Metabólica Fase II/genética
Ligação Proteica
Caracteres Sexuais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Analgesics, Non-Narcotic); 0 (Glucuronides); 362O9ITL9D (Acetaminophen); 64014-06-8 (acetaminophen cysteine); EC 2.4.1.17 (Glucuronosyltransferase); EC 2.4.1.17 (UDP-glucuronosyltransferase 2B15, human); K848JZ4886 (Cysteine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170902
[Lr] Data última revisão:
170902
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170701
[St] Status:MEDLINE
[do] DOI:10.1124/jpet.117.242107


  10 / 6887 MEDLINE  
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[PMID]:28637770
[Au] Autor:Matic M; de Wildt SN; Tibboel D; van Schaik RHN
[Ad] Endereço:Department of Clinical Chemistry, Erasmus University Medical Center, Rotterdam, the Netherlands.
[Ti] Título:Analgesia and Opioids: A Pharmacogenetics Shortlist for Implementation in Clinical Practice.
[So] Source:Clin Chem;63(7):1204-1213, 2017 Jul.
[Is] ISSN:1530-8561
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The use of opioids to alleviate pain is complicated by the risk of severe adverse events and the large variability in dose requirements. Pharmacogenetics (PGx) could possibly be used to tailor pain medication based on an individual's genetic background. Many potential genetic markers have been described, and the importance of genetic predisposition in opioid efficacy and toxicity has been demonstrated in knockout mouse models and human twin studies. Such predictors are especially of value for neonates and young children, in whom the assessment of efficacy or side effects is complicated by the inability of the patient to communicate this properly. The current problem is determining which of the many potential candidates to focus on for clinical implementation. CONTENT: We systematically searched publications on PGx for opioids in 5 databases, aiming to identify PGx markers with sufficient robust data and high enough occurrence for potential clinical application. The initial search yielded 4257 unique citations, eventually resulting in 852 relevant articles covering 24 genes. From these genes, we evaluated the evidence and selected the most promising 10 markers: cytochrome P450 family 2 subfamily D member 6 ( ), cytochrome P450 family 3 subfamily A member 4 ( ), cytochrome P450 family 3 subfamily A member 5 ( ), UDP glucuronosyltransferase family 2 member B7 ( ), ATP binding cassette subfamily B member 1 ( ), ATP binding cassette subfamily C member 3 ( ), solute carrier family 22 member 1 ( ), opioid receptor kappa 1 ( ), catechol- -methyltransferase ( ), and potassium voltage-gated channel subfamily J member 6 ( ). Treatment guidelines based on genotype are already available only for . SUMMARY: The application of PGx in the management of pain with opioids has the potential to improve therapy. We provide a shortlist of 10 genes that are the most promising markers for clinical use in this context.
[Mh] Termos MeSH primário: Analgésicos Opioides/uso terapêutico
Dor/tratamento farmacológico
Farmacogenética/tendências
[Mh] Termos MeSH secundário: Membro 1 da Subfamília B de Cassetes de Ligação de ATP/genética
Analgésicos Opioides/farmacologia
Variação Genética
Glucuronosiltransferase/genética
Seres Humanos
Manejo da Dor
Farmacogenética/normas
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (ATP-Binding Cassette, Sub-Family B, Member 1); 0 (Analgesics, Opioid); EC 2.4.1.17 (Glucuronosyltransferase); EC 2.4.1.17 (UGT2A1 protein, human)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170623
[St] Status:MEDLINE
[do] DOI:10.1373/clinchem.2016.264986



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