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[PMID]:9851889
[Au] Autor:Whitin JC; Tham DM; Bhamre S; Ornt DB; Scandling JD; Tune BM; Salvatierra O; Avissar N; Cohen HJ
[Ad] Endereço:Department of Pediatrics, Stanford University Medical Center, Stanford, California, 94305, USA. John.Whitin@Forsythe.Stanford.Edu
[Ti] Título:Plasma glutathione peroxidase and its relationship to renal proximal tubule function.
[So] Source:Mol Genet Metab;65(3):238-45, 1998 Nov.
[Is] ISSN:1096-7192
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Selenium-dependent extracellular glutathione peroxidase (E-GPx) is found in plasma and other extracellular fluids. Previous studies have indicated that patients with chronic renal failure on dialysis have low plasma GPx activity. In this study, dialysis patients had approximately 40% of control plasma GPx activity, while anephric individuals had lowest plasma GPx activities ranging from 2 to 22% of control. The residual plasma GPx activity in anephric individuals could be completely precipitated by anti-E-GPx antibodies, indicating that all plasma GPx activity can be attributed to E-GPx in both normal and anephric individuals. Plasma GPx activity rises rapidly following kidney transplantation, often reaching normal values within 10 days. The plasma GPx activity in some transplanted patients rises to levels higher than the normal range, followed by a return to the normal range. Since E-GPx in the kidney is primarily synthesized in the proximal tubules, we investigated whether nephrotoxic agents known to disrupt proximal tubule function also affected plasma GPx activity. The beta-lactam antibiotic cephaloglycin rapidly caused a decrease in plasma GPx activity in rabbits. In addition, the chemotherapeutic agent ifosfamide caused a decrease in plasma GPx activity in pediatric osteosarcoma patients. Fanconi syndrome associated with either ifosfamide therapy or valproic acid therapy also caused a decrease in plasma GPx activity. Thus plasma GPx activity is related to kidney function and is decreased in certain situations where nephrotoxic drugs are administered. Monitoring plasma GPx activity may have predictive value in evaluating the function of transplanted kidneys or in predicting those patients particularly at risk of nephrotoxic injury associated with certain medications.
[Mh] Termos MeSH primário: Glutationa Peroxidase/sangue
Nefropatias/enzimologia
Túbulos Renais Proximais/fisiologia
[Mh] Termos MeSH secundário: Adulto
Animais
Anticorpos/farmacologia
Cefaloglicina/efeitos adversos
Cefaloglicina/farmacologia
Cefaloglicina/uso terapêutico
Criança
Creatinina/sangue
Síndrome de Fanconi/induzido quimicamente
Glutationa Peroxidase/imunologia
Seres Humanos
Ifosfamida/efeitos adversos
Ifosfamida/farmacologia
Ifosfamida/uso terapêutico
Transplante de Rim
Túbulos Renais Proximais/efeitos dos fármacos
Nefrectomia
Osteossarcoma/induzido quimicamente
Osteossarcoma/tratamento farmacológico
Coelhos
Ácido Valproico/efeitos adversos
Ácido Valproico/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, U.S. GOV'T, P.H.S.
[Nm] Nome de substância:
0 (Antibodies); 614OI1Z5WI (Valproic Acid); AYI8EX34EU (Creatinine); EC 1.11.1.9 (Glutathione Peroxidase); NE7R11LA95 (Cephaloglycin); UM20QQM95Y (Ifosfamide)
[Em] Mês de entrada:9902
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:981216
[St] Status:MEDLINE


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[PMID]:8619902
[Au] Autor:Tune BM; Hsu CY; Fravert D
[Ad] Endereço:Department of Pediatrics, Stanford University, School of Medicine, CA, USA.
[Ti] Título:Cephalosporin and carbacephem nephrotoxicity. Roles of tubular cell uptake and acylating potential.
[So] Source:Biochem Pharmacol;51(4):557-61, 1996 Feb 23.
[Is] ISSN:0006-2952
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Three beta-lactams, desacetylcephaloglycin, ampicillin, and loracarbef, were studied to test a hypothesis derived from retrospective analysis of previously studied cephalosporins: that beta-lactam nephrotoxicity develops in approximate proportion to tubular cell antibiotic concentrations and lactam ring reactivities. Concentrations of each beta-lactam (and insulin) in rabbit renal cortex and serum were measured at the end of 0.5-hr infusions of 100 mg antibiotic/kg body weight and 0.5 to 0.67 hr later. Total cortical AUCs (total areas under the curve of concentration and time in renal cortex) and transported cortical AUCs (total minus insulin-space beta lactam) were calculated from these measurements. Reactivities, determined by the rate constants of lactam-ring opening at pH 10, were taken from the literature. Nephrotoxicity was quantified by grades of proximal tubular cell necrosis and by serum creatinine concentrations 2 days after infusion of 100-1500 mg/kg of the antibiotics. Desacetylcephaloglycin was slightly less nephrotoxic than cephaloglycin; the AUCs reactivities, and toxicities of these two cephalosporins fit the proposed model, particularly when allowance is made for hepatic and renal deacetylation of cephaloglycin. The very low AUCs, limited reactivity, and absence of nephrotoxicity of ampicillin also fit the model. Loracarbef had a transported AUC less than three times, and reactivity one-thirtieth, those of cefaclor, respectively. Although only at 1500 mg/kg, loracarbef was significantly more nephrotic than cefaclor. If the relativity of loracarbef with its targeted bacterial proteins, which is essentially the same as that of cefaclor, is considered instead of the base hydrolysis rate constant, than loracarbef also fits the model. By the same analysis, the comparatively high in vitro stability of other carbacephems, although pharmaceutically convenient, may not limit their nephrotoxicity.
[Mh] Termos MeSH primário: Ampicilina/farmacocinética
Ampicilina/toxicidade
Cefaloglicina/análogos & derivados
Cefalosporinas/farmacocinética
Cefalosporinas/toxicidade
Rim/efeitos dos fármacos
[Mh] Termos MeSH secundário: Acilação
Ampicilina/sangue
Animais
Antibacterianos/farmacocinética
Antibacterianos/toxicidade
Transporte Biológico
Cefaloglicina/sangue
Cefaloglicina/farmacocinética
Cefaloglicina/toxicidade
Cefalosporinas/sangue
Meia-Vida
Infusões Intravenosas
Rim/metabolismo
Rim/patologia
Córtex Renal/metabolismo
Penicilinas/sangue
Penicilinas/farmacocinética
Penicilinas/toxicidade
Coelhos
Relação Estrutura-Atividade
Distribuição Tecidual
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, U.S. GOV'T, P.H.S.
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); 0 (Cephalosporins); 0 (Penicillins); 0 (desacetylcephaloglycin); 3X11EVM5SU (loracarbef); 7C782967RD (Ampicillin); NE7R11LA95 (Cephaloglycin)
[Em] Mês de entrada:9606
[Cu] Atualização por classe:141120
[Lr] Data última revisão:
141120
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:960223
[St] Status:MEDLINE


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[PMID]:7887988
[Au] Autor:Tune BM; Hsu CY
[Ad] Endereço:Department of Pediatrics, Stanford University School of Medicine, CA 94305-5119.
[Ti] Título:Toxicity of cephalosporins to fatty acid metabolism in rabbit renal cortical mitochondria.
[So] Source:Biochem Pharmacol;49(5):727-34, 1995 Mar 01.
[Is] ISSN:0006-2952
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:UNLABELLED: Cephaloglycin (Cgl) and cephaloridine (Cld) are acutely toxic to the proximal renal tubule, in part because of their cellular uptake by a contraluminal anionic secretory carrier and in part through their intracellular attack on the mitochondrial transport and oxidation of tricarboxylic acid (TCA) cycle anionic substrates. Preliminary studies with Cgl have provided evidence of a role of fatty acid (FA) metabolism in its nephrotoxicity, and work with Cld has shown it to be a potent inhibitor of renal tubular cell and mitochondrial carnitine (Carn) transport. Studies were therefore done to examine the effects of Cgl and Cld on the mitochondrial metabolism of butyrate, the anion of a short-chain FA that does not require the Carn shuttle to enter the inner matrix, and the effects of Cgl on the metabolism of palmitoylcarnitine (PCarn), the Carn conjugate of a long-chain FA that does enter the mitochondrion by the Carn shuttle. The following was found: (1) Cgl reduced the oxidation and uptake of butyrate after in vitro (2000 micrograms/mL, immediate effect) and after in vivo (300 mg/kg body weight, 1 hr before killing) exposure; (2) Cld caused milder in vitro toxicity, and no significant in vivo toxicity, to mitochondrial butyrate metabolism; (3) like Cld, Cgl reduced PCarn-mediated respiration after in vivo exposure, but, unlike Cld, it did not inhibit respiration with PCarn in vitro; (4) the Carn carrier was stimulated slightly by in vitro Cgl but was unaffected by in vivo Cgl; (5) in vivo Cgl had no effect on mitochondrial free Carn or long-chain acylCarn concentrations in the in situ kidney; (6) Cgl increased the excretion of Carn minimally compared with the effect of Cld; and (7) cephalexin, a nontoxic cephalosporin, caused mild reductions of respiration with butyrate and PCarn during in vitro exposure, but stimulated respiration with both substrates after in vivo exposure. CONCLUSIONS: Cgl has essentially the same patterns of in vitro and in vivo toxicity against mitochondrial butyrate uptake and oxidation that both Cgl and Cld have against TCA-cycle substrates. Cld has little or no in vivo toxicity to mitochondrial butyrate metabolism, whereas in vivo Cgl is as toxic as Cld to respiration with PCarn. The greater overall in vivo toxicity of Cgl to mitochondrial FA metabolism, with lower cortical concentrations and AUCs than those of Cld, supports earlier evidence that Cld is less toxic than Cgl at the molecular level.
[Mh] Termos MeSH primário: Carnitina/metabolismo
Cefalosporinas/toxicidade
Ácidos Graxos/metabolismo
Córtex Renal/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Butiratos/metabolismo
Ácido Butírico
Carnitina/urina
Cefalexina/toxicidade
Cefaloglicina/toxicidade
Cefaloridina/toxicidade
Córtex Renal/metabolismo
Mitocôndrias/efeitos dos fármacos
Mitocôndrias/metabolismo
Palmitoilcarnitina/metabolismo
Coelhos
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, U.S. GOV'T, P.H.S.
[Nm] Nome de substância:
0 (Butyrates); 0 (Cephalosporins); 0 (Fatty Acids); 107-92-6 (Butyric Acid); 1935-18-8 (Palmitoylcarnitine); LVZ1VC61HB (Cephaloridine); NE7R11LA95 (Cephaloglycin); OBN7UDS42Y (Cephalexin); S7UI8SM58A (Carnitine)
[Em] Mês de entrada:9504
[Cu] Atualização por classe:151119
[Lr] Data última revisão:
151119
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:950301
[St] Status:MEDLINE


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[PMID]:7565098
[Au] Autor:Lepage S; Lakaye B; Galleni M; Thamm I; Crine M; Groslambert S; Frère JM
[Ad] Endereço:Laboratoire d'Enzymologie et Centre d'Ingénierie des Protéines, Université de Liège, Sart Tilman, Belgium.
[Ti] Título:Saturation of penicillin-binding protein 1 by beta-lactam antibiotics in growing cells of Bacillus licheniformis.
[So] Source:Mol Microbiol;16(2):365-72, 1995 Apr.
[Is] ISSN:0950-382X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:With the help of a new highly sensitive method allowing the quantification of free penicillin-binding proteins (PBPs) and of an integrated mathematical model, the progressive saturation of PBP1 by various beta-lactam antibiotics in growing cells of Bacillus licheniformis was studied. Although the results confirmed PBP1 as a major lethal target for these compounds, they also underlined several weaknesses in our present understanding of this phenomenon. In growing cells, but not in resting cells, the penicillin target(s) appeared to be somewhat protected from the action of the inactivators. In vitro experiments indicated that amino acids, peptides and depsipeptides mimicking the peptide moiety of the nascent peptidoglycan significantly interfered with the acylation of PBP1 by the antibiotics. In addition, the level of PBP1 saturation at antibiotic concentrations corresponding to the minimum inhibitory concentrations was not constant, suggesting that additional, presently undiscovered, factors might be necessary to account for the experimental observations.
[Mh] Termos MeSH primário: Antibacterianos/metabolismo
Bacillus/metabolismo
Proteínas de Bactérias
Proteínas de Transporte/metabolismo
Hexosiltransferases
Muramilpentapeptídeo Carboxipeptidase/metabolismo
Penicilinas/metabolismo
Peptidil Transferases
[Mh] Termos MeSH secundário: Acilação
Aminoácidos/metabolismo
Antibacterianos/farmacologia
Bacillus/crescimento & desenvolvimento
Cefaloglicina/metabolismo
Cefalosporinas/metabolismo
Cloxacilina/metabolismo
Ésteres/metabolismo
Cinética
Testes de Sensibilidade Microbiana
Modelos Moleculares
Proteínas de Ligação às Penicilinas
Peptídeos/metabolismo
Especificidade por Substrato
Compostos de Sulfidrila/metabolismo
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Amino Acids); 0 (Anti-Bacterial Agents); 0 (Bacterial Proteins); 0 (Carrier Proteins); 0 (Cephalosporins); 0 (Esters); 0 (Penicillin-Binding Proteins); 0 (Penicillins); 0 (Peptides); 0 (Sulfhydryl Compounds); 3XIY7HJT5L (cephalosporin C); EC 2.3.2.12 (Peptidyl Transferases); EC 2.4.1.- (Hexosyltransferases); EC 3.4.17.8 (Muramoylpentapeptide Carboxypeptidase); NE7R11LA95 (Cephaloglycin); O6X5QGC2VB (Cloxacillin)
[Em] Mês de entrada:9510
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:950401
[St] Status:MEDLINE


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[PMID]:2133431
[Au] Autor:Tune BM; Hsu CY
[Ad] Endereço:Department of Pediatrics, Stanford University School of Medicine, CA 94305.
[Ti] Título:The renal mitochondrial toxicity of beta-lactam antibiotics: in vitro effects of cephaloglycin and imipenem.
[So] Source:J Am Soc Nephrol;1(5):815-21, 1990 Nov.
[Is] ISSN:1046-6673
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The nephrotoxic beta-lactam antibiotics cephaloridine, cephaloglycin, and imipenem produce irreversible injury to renal mitochondrial anionic substrate uptake and respiration after 1 to 2 h of in vivo exposure. Toxicity during in vitro exposure is nearly identical but is immediate in onset and is reversed by the mitochondria being washed or the substrate concentrations being increased. A model of injury that accounts for these findings proposes that the beta-lactams fit carriers for mitochondrial substrate uptake, causing inhibition that is initially reversible and becomes irreversible as the antibiotics acylate the transporters. These studies were designed to create an environment of prolonged in vitro exposure, first, to determine whether toxicity becomes irreversible with time and, second, to study the molecular properties of toxicity. Respiration with and the uptake of succinate and ADP were measured in rabbit renal cortical mitochondria exposed for 2 to 6 h to 300 to 3,000 micrograms of cephalexin (nontoxic) or cephaloglycin or imipenem (nephrotoxic) per mL and then washed to remove the antibiotic. In vitro cephalexin reduced respiration only slightly and was therefore not studied further. Cephaloglycin and imipenem irreversibly reduced both respiration and succinate uptake. ADP uptake was unaffected by cephaloglycin and was slightly reduced by imipenem. Finally, cilastatin, which prevents the tubular necrosis produced by imipenem in vivo, reduced its mitochondrial toxicity in vitro. It is concluded that the pattern of in vitro injury of the nephrotoxic beta-lactams to mitochondrial substrate uptake and respiration evolves in a time-dependent and concentration-dependent manner, consistent with the proposed model of acylation and inactivation of substrate transporters, and that the protective action of cilastatin against imipenem occurs at least partly at a subcellular level.
[Mh] Termos MeSH primário: Antibacterianos/farmacologia
Cefaloglicina/farmacologia
Imipenem/farmacologia
Rim/efeitos dos fármacos
Mitocôndrias/efeitos dos fármacos
[Mh] Termos MeSH secundário: Difosfato de Adenosina/metabolismo
Animais
Transporte Biológico
Cilastatina/farmacologia
Mitocôndrias/metabolismo
Concentração Osmolar
Consumo de Oxigênio
Succinatos/metabolismo
Ácido Succínico
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, P.H.S.
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); 0 (Succinates); 141A6AMN38 (Cilastatin); 61D2G4IYVH (Adenosine Diphosphate); 71OTZ9ZE0A (Imipenem); AB6MNQ6J6L (Succinic Acid); NE7R11LA95 (Cephaloglycin)
[Em] Mês de entrada:9203
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:901101
[St] Status:MEDLINE


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[PMID]:1980443
[Au] Autor:Mendizabal MV; Idoate I; Larralde J
[Ad] Endereço:Departamento de Fisiología y Nutrición, Facultad de Farmacia, Universidad de Navarra, Pamplona, España.
[Ti] Título:Effect of cefatrizine and cephaloglycine on L-leucine absorption in rat jejunum.
[So] Source:Comp Biochem Physiol C;96(2):317-20, 1990.
[Is] ISSN:0742-8413
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:1. The oral cephalosporins: cefatrizine and cephaloglycine inhibit the L-leucine absorption in vivo on rat jejunum. 2. This inhibition is dose and time dependent and the effect is irreversible. 3. These antibiotics have a systemic effect on L-leucine absorption. 4. The inhibition of these antibiotics affect only leucine transport, without affecting the diffusion. 5. Cefatrizine and cephaloglycine inhibit the basolateral (Na(+)-K+) ATPase activity in rat jejunum.
[Mh] Termos MeSH primário: Cefatrizina/farmacologia
Cefaloglicina/farmacologia
Absorção Intestinal/efeitos dos fármacos
Jejuno/metabolismo
Leucina/farmacocinética
[Mh] Termos MeSH secundário: Animais
Transporte Biológico Ativo/efeitos dos fármacos
Masculino
Ratos
Ratos Endogâmicos
ATPase Trocadora de Sódio-Potássio/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
8P4W949T8K (Cefatrizine); EC 3.6.3.9 (Sodium-Potassium-Exchanging ATPase); GMW67QNF9C (Leucine); NE7R11LA95 (Cephaloglycin)
[Em] Mês de entrada:9103
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:900101
[St] Status:MEDLINE


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[PMID]:2930580
[Au] Autor:Tune BM; Fravert D; Hsu CY
[Ad] Endereço:Department of Pediatrics, Stanford University, School of Medicine, CA 94305.
[Ti] Título:Oxidative and mitochondrial toxic effects of cephalosporin antibiotics in the kidney. A comparative study of cephaloridine and cephaloglycin.
[So] Source:Biochem Pharmacol;38(5):795-802, 1989 Mar 01.
[Is] ISSN:0006-2952
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Cephaloridine and cephaloglycin are the two most nephrotoxic cephalosporins released for human use. Cephaloridine has been shown to produce both oxidative and mitochondrial respiratory injury in renal cortex in patterns of dose (or concentration) and time that are consistent with pathogenicity. Cephaloglycin also produces respiratory toxicity, and recent studies have provided evidence that this injury results from an inactivation of mitochondrial anionic substrate transporters. The abilities of cephaloglycin to produce oxidative changes and cephaloridine to block mitochondrial substrate uptake have not been examined yet. We therefore compared these two cephalosporins with one another and with cephalexin, which is not nephrotoxic, in the production of the following: (1) several components of oxidative stress or damage [depletion of reduced glutathione (GSH) and production of oxidized glutathione (GSSG) in renal cortex, inhibition of glutathione reductase in vitro, and production of the lipid peroxidation products malondialdehyde (MDA) and conjugated dienes (CDs) in renal cortex]; and (2) renal cortical mitochondrial toxicity [to both respiration with, and the transport of, succinate]. Cephaloridine depleted GSH and elevated GSSG in renal cortex, inhibited glutathione reductase, and increased both MDA in whole cortex and CDs in cortical microsomes and mitochondria. While cephaloglycin depleted GSH at least as much as did cephaloridine, it produced one-fifth as much GSSG and had little or no effect on glutathione reductase activity or on cortical MDA or microsomal CDs; cephaloglycin caused a transient small increase of mitochondrial CDs. Cephalexin produced no oxidative changes except for a slight increase of mitochondrial CDs comparable to that produced by cephaloglycin. Both cephaloridine and cephaloglycin, but not cephalexin, decreased the unidirectional uptake of, and respiration with, succinate in cortical mitochondria. We conclude that cephaloridine and cephaloglycin are both toxic to mitochondrial substrate uptake and respiration, but differ significantly in their generation of products of oxidation.
[Mh] Termos MeSH primário: Cefaloglicina/toxicidade
Cefaloridina/toxicidade
Rim/efeitos dos fármacos
Mitocôndrias/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Feminino
Glutationa/metabolismo
Glutationa Redutase/antagonistas & inibidores
Peroxidação de Lipídeos/efeitos dos fármacos
Mitocôndrias/metabolismo
Consumo de Oxigênio/efeitos dos fármacos
Coelhos
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, P.H.S.
[Nm] Nome de substância:
EC 1.8.1.7 (Glutathione Reductase); GAN16C9B8O (Glutathione); LVZ1VC61HB (Cephaloridine); NE7R11LA95 (Cephaloglycin)
[Em] Mês de entrada:8904
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:890301
[St] Status:MEDLINE


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[PMID]:3220913
[Au] Autor:Blanchin MD; Rondot-Dudragne ML
[Ad] Endereço:Laboratoire de Chimie Analytique et Toxicologie, Faculté de Pharmacie, Montpellier, France.
[Ti] Título:[Determination of cefaloglycine and cefroxadin in biological media with thin layer chromatography with fluorometric detection].
[Ti] Título:Détermination de la céfaloglycine et de la céfroxadine dans les milieux biologiques par chromatographie sur couche mince avec détection fluorimétrique..
[So] Source:J Chromatogr;432:407-11, 1988 Nov 18.
[Cp] País de publicação:Netherlands
[La] Idioma:fre
[Mh] Termos MeSH primário: Cefaloglicina/análise
Cefalosporinas/análise
Cefradina/análise
[Mh] Termos MeSH secundário: Cefaloglicina/sangue
Cefaloglicina/urina
Cefradina/análogos & derivados
Cefradina/sangue
Cefradina/urina
Cromatografia em Camada Delgada
Seres Humanos
Padrões de Referência
Espectrometria de Fluorescência
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cephalosporins); B908C4MV2R (cefroxadine); F1BC02I72W (Cephradine); NE7R11LA95 (Cephaloglycin)
[Em] Mês de entrada:8903
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:881118
[St] Status:MEDLINE


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PubMed Central Texto completo
[PMID]:3456343
[Au] Autor:Pucci MJ; Hinks ET; Dicker DT; Higgins ML; Daneo-Moore L
[Ti] Título:Inhibition of beta-lactam antibiotics at two different times in the cell cycle of Streptococcus faecium ATCC 9790.
[So] Source:J Bacteriol;165(3):682-8, 1986 Mar.
[Is] ISSN:0021-9193
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Treatment of Streptococcus faecium ATCC 9790 with sublytic concentrations of beta-lactam antibiotics revealed two different division blocks in the cell division cycle. One block, induced by N-formimidoyl thienamycin and methicillin, occurred before the completion of chromosome replication, whereas the other, induced by cefoxitin and cephalothin, took place later in the cycle. In addition, these antibiotics gave rise to distinct morphological forms; the antibiotics acting at the earlier block point produced mainly "dumbbells," whereas those affecting the later time formed "lemons." When used in combination N-formimidoyl thienamycin and cefoxitin exerted synergistic killing on this strain. These data suggest that beta-lactam antibiotics have at least two sites of action in S. faecium.
[Mh] Termos MeSH primário: Antibacterianos/farmacologia
Streptococcus/efeitos dos fármacos
[Mh] Termos MeSH secundário: Cefoxitina/farmacologia
Divisão Celular/efeitos dos fármacos
Cefaloglicina/farmacologia
Cefalotina/farmacologia
Sinergismo Farmacológico
Imipenem
Microscopia Eletrônica de Varredura
Streptococcus/crescimento & desenvolvimento
Streptococcus/ultraestrutura
Tienamicinas/farmacologia
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, U.S. GOV'T, P.H.S.
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); 0 (Thienamycins); 6OEV9DX57Y (Cefoxitin); 71OTZ9ZE0A (Imipenem); NE7R11LA95 (Cephaloglycin); R72LW146E6 (Cephalothin)
[Em] Mês de entrada:8604
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:860301
[St] Status:MEDLINE


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[PMID]:3082924
[Au] Autor:Chen KC; Holmes KK
[Ti] Título:Enhancement of fluorescence development of end products by use of a fluorescence developer solution in a rapid and sensitive fluorescent spot test for specific detection of microbial beta-lactamases.
[So] Source:J Clin Microbiol;23(3):539-44, 1986 Mar.
[Is] ISSN:0095-1137
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A fluorescent spot test method for specific detection of microbial beta-lactamases as previously published (K. C. S. Chen, J. S. Knapp, and K. K. Holmes, J. Clin. Microbiol. 19:818-825, 1984) was improved by the use of a fluorescence developer solution. The fluorescence developer solution used in this study consisted of 0.78 M sodium tartrate buffer containing 12% formaldehyde at a final pH of 4.5. An addition of 1 volume of fluorescence developer solution to 5 volumes of ampicillin or cephalex substrate solution incubated with beta-lactamase-producing organisms, followed by heating the mixture at 45 degrees C for 10 min resulted in enhancement of fluorescence of the end products of beta-lactamase activity. This provides a more sensitive assay for microbial beta-lactamases and offers the potential for direct detection of beta-lactamases in clinical specimens.
[Mh] Termos MeSH primário: Ampicilina/metabolismo
Bactérias/enzimologia
Cefalexina/metabolismo
beta-Lactamases/análise
[Mh] Termos MeSH secundário: Amidoidrolases/metabolismo
Amoxicilina/metabolismo
Cefadroxila/metabolismo
Cefaloglicina/metabolismo
Cefalosporinase/metabolismo
Enterobacter/enzimologia
Fluorescência
Haemophilus influenzae/enzimologia
Temperatura Alta
Neisseria gonorrhoeae/enzimologia
Penicilinase/metabolismo
Staphylococcus aureus/enzimologia
beta-Lactamases/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, U.S. GOV'T, P.H.S.
[Nm] Nome de substância:
280111G160 (Cefadroxil); 7C782967RD (Ampicillin); 804826J2HU (Amoxicillin); EC 3.5.- (Amidohydrolases); EC 3.5.1.4 (amidase); EC 3.5.2.- (Cephalosporinase); EC 3.5.2.- (Penicillinase); EC 3.5.2.6 (beta-Lactamases); NE7R11LA95 (Cephaloglycin); OBN7UDS42Y (Cephalexin)
[Em] Mês de entrada:8605
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:860301
[St] Status:MEDLINE



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