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[PMID]:27925185
[Au] Autor:Pace E; Di Vincenzo S; Ferraro M; Siena L; Chiappara G; Dino P; Vitulo P; Bertani A; Saibene F; Lanata L; Gjomarkaj M
[Ad] Endereço:Institute of Biomedicine and Molecular Immunology, Consiglio Nazionale delle Ricerche, Palermo, Italy.
[Ti] Título:Effects of Carbocysteine and Beclomethasone on Histone Acetylation/Deacetylation Processes in Cigarette Smoke Exposed Bronchial Epithelial Cells.
[So] Source:J Cell Physiol;232(10):2851-2859, 2017 Oct.
[Is] ISSN:1097-4652
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Histone deacetylase expression/activity may control inflammation, cell senescence, and responses to corticosteroids. Cigarette smoke exposure, increasing oxidative stress, may negatively affect deacetylase expression/activity. The effects of cigarette smoke extracts (CSE), carbocysteine, and beclomethasone dipropionate on chromatin remodeling processes in human bronchial epithelial cells are largely unknown. The present study was aimed to assess the effects of cigarette smoke, carbocysteine, and beclomethasone dipropionate on histone deacetylase 3 (HDAC3) expression/activity, N-CoR (nuclear receptor corepressor) expression, histone acetyltransferases (HAT) (p300/CBP) expression, p-CREB and IL-1 m-RNA expression, neutrophil chemotaxis. Increased p-CREB expression was observed in the bronchial epithelium of smokers. CSE increased p-CREB expression and decreased HDAC3 expression and activity and N-CoR m-RNA and protein expression. At the same time, CSE increased the expression of the HAT, p300/CBP. All these events increased acetylation processes within the cells and were associated to increased IL-1 m-RNA expression and neutrophil chemotaxis. The incubation of CSE exposed cells with carbocysteine and beclomethasone counteracted the effects of cigarette smoke on HDAC3 and N-CoR but not on p300/CBP. The increased deacetylation processes due to carbocysteine and beclomethasone dipropionate incubation is associated to reduced p-CREB, IL-1 m-RNA expression, neutrophil chemotaxis. These findings suggest a new role of combination therapy with carbocysteine and beclomethasone dipropionate in restoring deacetylation processes compromised by cigarette smoke exposure. J. Cell. Physiol. 232: 2851-2859, 2017. © 2016 Wiley Periodicals, Inc.
[Mh] Termos MeSH primário: Beclometasona/farmacologia
Brônquios/efeitos dos fármacos
Carbocisteína/farmacologia
Proteína p300 Associada a E1A/metabolismo
Células Epiteliais/efeitos dos fármacos
Histona Desacetilases/metabolismo
Histonas/metabolismo
Processamento de Proteína Pós-Traducional
Fumaça/efeitos adversos
Fumar/efeitos adversos
[Mh] Termos MeSH secundário: Acetilação
Brônquios/enzimologia
Brônquios/patologia
Linhagem Celular
Quimiotaxia de Leucócito/efeitos dos fármacos
Proteína de Ligação ao Elemento de Resposta ao AMP Cíclico/metabolismo
Citoproteção
Células Epiteliais/enzimologia
Células Epiteliais/patologia
Seres Humanos
Interleucina-1/genética
Interleucina-1/metabolismo
Neutrófilos/efeitos dos fármacos
Neutrófilos/metabolismo
Correpressor 1 de Receptor Nuclear/genética
Correpressor 1 de Receptor Nuclear/metabolismo
Fosforilação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CREB1 protein, human); 0 (Cyclic AMP Response Element-Binding Protein); 0 (Histones); 0 (Interleukin-1); 0 (NCOR1 protein, human); 0 (Nuclear Receptor Co-Repressor 1); 0 (Smoke); 740J2QX53R (Carbocysteine); EC 2.3.1.48 (E1A-Associated p300 Protein); EC 2.3.1.48 (EP300 protein, human); EC 3.5.1.98 (Histone Deacetylases); EC 3.5.1.98 (histone deacetylase 3); KGZ1SLC28Z (Beclomethasone)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170919
[Lr] Data última revisão:
170919
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161208
[St] Status:MEDLINE
[do] DOI:10.1002/jcp.25710


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[PMID]:27328977
[Au] Autor:Song Y; Yu P; Lu JJ; Lu HZ; Zhu L; Yu ZH; Chen HZ; Cui YY
[Ad] Endereço:Department of Pharmacology, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.
[Ti] Título:A mucoactive drug carbocisteine ameliorates steroid resistance in rat COPD model.
[So] Source:Pulm Pharmacol Ther;39:38-47, 2016 Aug.
[Is] ISSN:1522-9629
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Steroid insensitivity has been commonly found in chronic obstructive pulmonary disease (COPD) patients, which is mediated by the reduction of histone deacetylase (HDAC) 2. Here we aimed to establish a steroid resistant model on experimental COPD rats and evaluate the effect of carbocisteine (S-CMC), a mucoactive drug. Exposure to cigarette smoke (CS) caused marked pathological features of COPD which are insensitive to DEX associated with the down-regulation of HDAC2 expression/activity. The DEX insensitivity observed in COPD featured rats was improved by S-CMC in the aspects of inhibiting chronic lung inflammation (total and differential inflammatory cell counts, inflammatory cytokines release and inflammatory cells infiltration); ameliorating airway remodeling (thickness of airway epithelium and smooth muscle, airway fibrosis, and the level of α-SMA and TGF-ß1); improving emphysema (emphysema index D2, level of MMP-9 in BALF and the expression of alpha-1 antitrypsin) and preventing impairments of lung function (PEF, IP and IP-slope). Simultaneously, down-regulation of HDAC2 expression/activity was ameliorated by S-CMC treatment. These results indicate that the rat COPD model with steroid resistance was established by active smoking in a short time frame and demonstrate that the failure of steroid therapy can be restored by S-CMC accompanied by increasing HDAC2 expression/activity, providing additional evidence that S-CMC might be used for GC resistance in COPD.
[Mh] Termos MeSH primário: Carbocisteína/farmacologia
Dexametasona/farmacologia
Expectorantes/farmacologia
Doença Pulmonar Obstrutiva Crônica/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Citocinas/metabolismo
Modelos Animais de Doenças
Regulação para Baixo/efeitos dos fármacos
Resistência a Medicamentos
Feminino
Glucocorticoides/farmacologia
Histona Desacetilase 2/genética
Histona Desacetilase 2/metabolismo
Masculino
Doença Pulmonar Obstrutiva Crônica/etiologia
Doença Pulmonar Obstrutiva Crônica/fisiopatologia
Ratos
Ratos Sprague-Dawley
Testes de Função Respiratória
Fumar/efeitos adversos
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Expectorants); 0 (Glucocorticoids); 740J2QX53R (Carbocysteine); 7S5I7G3JQL (Dexamethasone); EC 3.5.1.98 (Histone Deacetylase 2)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160623
[St] Status:MEDLINE


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[PMID]:27237816
[Au] Autor:Pace E; Di Vincenzo S; Ferraro M; Bruno A; Dino P; Bonsignore MR; Battaglia S; Saibene F; Lanata L; Gjomarkaj M
[Ad] Endereço:Istituto di Biomedicina e Immunologia Molecolare, Consiglio Nazionale delle Ricerche, Palermo, Italy. Electronic address: pace@ibim.cnr.it.
[Ti] Título:Carbocysteine counteracts the effects of cigarette smoke on cell growth and on the SIRT1/FoxO3 axis in bronchial epithelial cells.
[So] Source:Exp Gerontol;81:119-28, 2016 Aug.
[Is] ISSN:1873-6815
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Cigarette smoke may accelerate cellular senescence by increasing oxidative stress. Altered proliferation and altered expression of anti-aging factors, including SIRT1 and FoxO3, characterise cellular senescence. The effects of carbocysteine on the SIRT1/FoxO3 axis and on downstream molecular mechanisms in human bronchial epithelial cells exposed to cigarette smoke are largely unknown. AIMS: Aim of this study was to explore whether carbocysteine modulated SIRT1/FoxO3 axis, and downstream molecular mechanisms associated to cellular senescence, in a bronchial epithelial cell line (16-HBE) exposed to cigarette smoke. METHODS: 16HBE cells were stimulated with/without cigarette smoke extracts (CSE) and carbocysteine. Flow cytometry and clonogenic assay were used to assess cell proliferation; western blot analysis was used for assessing nuclear expression of SIRT1 and FoxO3. The nuclear co-localization of SIRT1 and FoxO3 was assessed by fluorescence microscopy. Beta galactosidase (a senescence marker) and SIRT1 activity were assessed by specific staining and colorimetric assays, respectively. ChiP Assay and flow cytometry were used for assessing survivin gene regulation and protein expression, respectively. RESULTS: CSE decreased cell proliferation, the nuclear expression of SIRT1 and FoxO3 and increased beta galactosidase staining. CSE, reduced SIRT1 activity and FoxO3 localization on survivin promoter thus increasing survivin expression. In CSE stimulated bronchial epithelial cells carbocysteine reverted these phenomena by increasing cell proliferation, and SIRT1 and FoxO3 nuclear expression, and by reducing beta galactosidase staining and survivin expression. CONCLUSIONS: The study shows for the first time that carbocysteine may revert some senescence processes induced by oxidative stress due to cigarette smoke exposure.
[Mh] Termos MeSH primário: Carbocisteína/farmacologia
Proteína Forkhead Box O3/metabolismo
Sirtuína 1/metabolismo
Fumaça/efeitos adversos
Tabaco/efeitos adversos
[Mh] Termos MeSH secundário: Apoptose/efeitos dos fármacos
Linhagem Celular
Proliferação Celular/efeitos dos fármacos
Senescência Celular/efeitos dos fármacos
Células Epiteliais/efeitos dos fármacos
Proteína Forkhead Box O3/efeitos dos fármacos
Seres Humanos
Estresse Oxidativo/efeitos dos fármacos
Sirtuína 1/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (FOXO3 protein, human); 0 (Forkhead Box Protein O3); 0 (Smoke); 740J2QX53R (Carbocysteine); EC 3.5.1.- (SIRT1 protein, human); EC 3.5.1.- (Sirtuin 1)
[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:160531
[St] Status:MEDLINE


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[PMID]:26997568
[Au] Autor:Wang W; Guan WJ; Huang RQ; Xie YQ; Zheng JP; Zhu SX; Chen M; Zhong NS
[Ad] Endereço:State Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangzhou Institute of Respiratory Disease, First Affiliated Hospital of Guangzhou Medical University, Guangzhou 510120, China.
[Ti] Título:Carbocisteine attenuates TNF-α-induced inflammation in human alveolar epithelial cells in vitro through suppressing NF-κB and ERK1/2 MAPK signaling pathways.
[So] Source:Acta Pharmacol Sin;37(5):629-36, 2016 May.
[Is] ISSN:1745-7254
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:AIM: We previously proven that carbocisteine, a conventional mucolytic drug, remarkably reduced the rate of acute exacerbations and improved the quality of life in the patients with chronic obstructive pulmonary disease. In this study we investigated the mechanisms underlying the anti-inflammatory effects of carbocisteine in human alveolar epithelial cells in vitro. METHODS: Human lung adenocarcinoma cell line A549 was treated with TNF-α (10 ng/mL). Carbocisteine was administered either 24 h prior to or after TNF-α exposure. The cytokine release and expression were measured using ELISA and qRT-PCR. Activation of NF-κB was analyzed with Western blotting, immunofluorescence assay and luciferase reporter gene assay. The expression of ERK1/2 MAPK signaling proteins was assessed with Western blotting. RESULTS: Carbocisteine (10, 100, 1000 µmol/L), administered either before or after TNF-α exposure, dose-dependently suppressed TNF-α-induced inflammation in A549 cells, as evidenced by diminished release of IL-6 and IL-8, and diminished mRNA expression of IL-6, IL-8, TNF-α, MCP-1 and MIP-1ß. Furthermore, pretreatment with carbocisteine significantly decreased TNF-α-induced phosphorylation of NF-κB p65 and ERK1/2 MAPK, and inhibited the nuclear translocation of p65 subunit in A549 cells. In an NF-κB luciferase reporter system, pretreatment with carbocisteine dose-dependently inhibited TNF-α-induced transcriptional activity of NF-κB. CONCLUSION: Carbocisteine effectively suppresses TNF-α-induced inflammation in A549 cells via suppressing NF-κB and ERK1/2 MAPK signaling pathways.
[Mh] Termos MeSH primário: Células Epiteliais Alveolares/efeitos dos fármacos
Carbocisteína/farmacologia
Proteína Quinase 1 Ativada por Mitógeno/metabolismo
Proteína Quinase 3 Ativada por Mitógeno/metabolismo
NF-kappa B/metabolismo
Fator de Necrose Tumoral alfa/farmacologia
[Mh] Termos MeSH secundário: Células A549
Células Epiteliais Alveolares/metabolismo
Citocinas/metabolismo
Células HEK293
Seres Humanos
Inflamação/metabolismo
Transdução de Sinais
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (NF-kappa B); 0 (Tumor Necrosis Factor-alpha); 740J2QX53R (Carbocysteine); EC 2.7.11.24 (MAPK1 protein, human); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170228
[Lr] Data última revisão:
170228
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160322
[St] Status:MEDLINE
[do] DOI:10.1038/aps.2015.150


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[PMID]:26970503
[Au] Autor:Esposito A; Valentino MR; Bruzzese D; Bocchino M; Ponticiello A; Stanziola A; Sanduzzi A
[Ad] Endereço:Clinical Medicine and Surgery Department, School of Medicine, University of Naples Federico II, Italy. Electronic address: espositoantonella07@libero.it.
[Ti] Título:Effect of CArbocisteine in Prevention of exaceRbation of chronic obstructive pulmonary disease (CAPRI study): An observational study.
[So] Source:Pulm Pharmacol Ther;37:85-8, 2016 Apr.
[Is] ISSN:1522-9629
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Chronic Obstructive Pulmonary Disease (COPD) is a chronic and progressive lung disease characterized by irreversible airflow obstruction, airway inflammation, oxidative stress and, often, mucus hypersecretion. The aim of this study is to determine if carbocisteine, a mucolytic and antioxidant agent, administered daily for 12 months, can reduce exacerbation frequency in COPD patients. METHODS: This observational study was conducted in Naples (population approximately 1000,000), Italy. It included 85 out-patients (mean age of 67.8 ± 8.6 years) followed by Clinic of Respiratory Diseases of the University Federico II. Every patient underwent spirometry demonstrating airflow obstruction not fully reversible according to ERS/ATS criteria for COPD diagnosis (Tiffenau index less than 70% after administration of salbutamol, a beta2 agonist drug). Patients enrolled had diagnosed COPD since 2 years and suffered at least one exacerbation in the previous year. None of the patients had been treated with carbocisteine or other mucolytic agent for a longer period of time than 7 days and no more than 4 times in the previous year to the enrollment. All of them assumed daily 2.7 g of carbocisteine lysine salt for a year in addition to their basic therapy. RESULTS: The comparison of exacerbation frequency between the previous year (T0) and the end of study treatment (T12), documents a statistically significant reduction of exacerbations(number of exacerbations at T0: 2 [1,3] vs number of exacerbations at T12: 1 [1,2]; p < 0.001).Quality of life was also reported and showed a statistically significant improvement at the end of the study (p < 0.001).We did not find correlation between reducing exacerbation frequency and exposure to cigarette smoking, passive smoking exposure in childhood, the use of inhaled steroids, the level of education of our patients and the GOLD stadium. INTERPRETATION: Daily administration of a mucolytic drug such as carbocisteine for prolonged periods in addition to the bronchodilator therapy can be considered a good strategy for reducing exacerbation frequency in COPD.
[Mh] Termos MeSH primário: Carbocisteína/análogos & derivados
Expectorantes/uso terapêutico
Doença Pulmonar Obstrutiva Crônica/tratamento farmacológico
Qualidade de Vida
[Mh] Termos MeSH secundário: Idoso
Broncodilatadores/uso terapêutico
Carbocisteína/administração & dosagem
Carbocisteína/uso terapêutico
Expectorantes/administração & dosagem
Feminino
Seres Humanos
Itália
Masculino
Meia-Idade
Doença Pulmonar Obstrutiva Crônica/fisiopatologia
Fumar/epidemiologia
Espirometria
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE; OBSERVATIONAL STUDY
[Nm] Nome de substância:
0 (Bronchodilator Agents); 0 (Expectorants); 1D1Y95PXXA (carbocysteine-lysine); 740J2QX53R (Carbocysteine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171013
[Lr] Data última revisão:
171013
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160313
[St] Status:MEDLINE


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[PMID]:26849119
[Au] Autor:Wu K; Su X; Li G; Zhang N
[Ad] Endereço:Guangzhou Institute of Respiratory Disease, State Key Laboratory of Respiratory Diseases, The 1st Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, China.
[Ti] Título:Antioxidant Carbocysteine Treatment in Obstructive Sleep Apnea Syndrome: A Randomized Clinical Trial.
[So] Source:PLoS One;11(2):e0148519, 2016.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: This study aimed to examine the effects of carbocysteine in OSAS patients. METHODS: A total of 40 patients with moderate to severe obstructive sleep apnea syndrome (OSAS) were randomly divided into two groups. One group was treated with 1500 mg carbocysteine daily, and the other was treated with continuous positive airway pressure (CPAP) at night. Before treatment and after 6 weeks of treatment, all patients underwent polysomnography and completed questionnaires. Treatment compliance was compared between the two groups. Plasma was collected for various biochemical analyses. Endothelial function was assessed with ultrasound in the carbocysteine group. RESULTS: The proportion of patients who fulfilled the criteria for good compliance was higher in the carbocysteine group (n = 17) than in the CPAP group (n = 11; 100% vs. 64.7%). Compared with baseline values, the carbocysteine group showed significant improvement in their Epworth Sleepiness Scale score (10.18 ± 4.28 vs. 6.82 ± 3.66; P ≤ 0.01), apnea-hypopnea index (55.34 ± 25.03 vs. 47.56 ± 27.32; P ≤ 0.01), time and percentage of 90% oxygen desaturation (12.66 (2.81; 50.01) vs. 8.9 (1.41; 39.71); P ≤ 0.01), and lowest oxygen saturation level (65.88 ± 14.86 vs. 70.41 ± 14.34; P ≤ 0.01). Similar changes were also observed in the CPAP group. The CPAP group also showed a decreased oxygen desaturation index and a significant increase in the mean oxygen saturation after treatment, but these increases were not observed in the carbocysteine group. Snoring volume parameters, such as the power spectral density, were significantly reduced in both groups after the treatments. The plasma malondialdehyde level decreased and the superoxide dismutase and nitric oxide levels increased in both groups. The endothelin-1 level decreased in the CPAP group but did not significantly change in the carbocysteine group. Ultrasonography showed that the intima-media thickness decreased (0.71 ± 0.15 vs. 0.66 ± 0.15; P ≤ 0.05) but that flow-mediated dilation did not significantly change in the carbocysteine group. CONCLUSIONS: Oral carbocysteine slightly improves sleep disorders by attenuating oxidative stress in patients with moderate to severe OSAS. Carbocysteine may have a role in the treatment of OSAS patients with poor compliance with CPAP treatment. However, the efficiency and feasibility of carbocysteine treatment for OSAS needs further evaluation. TRIAL REGISTRATION: ClinicalTrials.gov NCT02015598.
[Mh] Termos MeSH primário: Antioxidantes/uso terapêutico
Carbocisteína/uso terapêutico
Apneia Obstrutiva do Sono/tratamento farmacológico
[Mh] Termos MeSH secundário: Adulto
Espessura Intima-Media Carotídea
Pressão Positiva Contínua nas Vias Aéreas
Endotelina-1/sangue
Seres Humanos
Masculino
Malondialdeído/sangue
Meia-Idade
Óxido Nítrico/sangue
Oxigênio/sangue
Polissonografia
Apneia Obstrutiva do Sono/diagnóstico
Ronco/tratamento farmacológico
Superóxido Dismutase/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antioxidants); 0 (Endothelin-1); 31C4KY9ESH (Nitric Oxide); 4Y8F71G49Q (Malondialdehyde); 740J2QX53R (Carbocysteine); EC 1.15.1.1 (Superoxide Dismutase); S88TT14065 (Oxygen)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:161215
[Lr] Data última revisão:
161215
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160206
[Cl] Clinical Trial:ClinicalTrial
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0148519


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[PMID]:26338263
[Au] Autor:Vandenbossche E; Lucas C; Mistry L; Garfield E; Mitchell SC; Steventon GB
[Ad] Endereço:a Department of Biochemistry and Physiology , School of Biosciences and Medicine, University of Surrey , Guildford , Surrey , UK and.
[Ti] Título:Phenylalanine monooxygenase and the sulfur oxygenation of S-carboxymethyl-L-cysteine in mice.
[So] Source:Xenobiotica;46(4):379-84, 2016.
[Is] ISSN:1366-5928
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:1. The extent of sulfoxidation of the drug, S-carboxymethyl-L-cysteine, has been shown to vary between individuals, with this phenomenon being mooted as a biomarker for certain disease states and susceptibilities. Studies in vitro have indicated that the enzyme responsible for this reaction was phenylalanine monooxygenase but to date no in vivo evidence exists to support this assumption. Using the mouse models of mild hyperphenylalaninamia (enu1 PAH variant) and classical phenylketonuria (enu2 PAH variant), the sulfur oxygenation of S-carboxymethyl-L-cysteine has been investigated. 2. Compared to the wild type (wt/wt) mice, both the heterozygous dominant (wt/enu1 and wt/enu2) mice and the homozygous recessive (enu1/enu1 and enu2/enu2) mice were shown to have significantly increased Cmax, AUC(0-180 min) and AUC(0-∞ min) values (15 - to 20-fold higher). These results were primarily attributable to the significantly reduced clearance of S-carboxymethyl-L-cysteine (13 - to 22-fold lower). 3. Only the wild type mice produced measurable quantities of the parent S-oxide metabolites. Those mice possessing one or more allelic variant showed no evidence of blood SCMC (R/S) S-oxides. These observations support the proposition that differences in phenylalanine hydroxylase activity underlie the variation in S-carboxymethyl-L-cysteine sulfoxidation and that no other enzyme is able to undertake this reaction.
[Mh] Termos MeSH primário: Carbocisteína/metabolismo
Oxigênio/metabolismo
Fenilalanina Hidroxilase/metabolismo
Enxofre/metabolismo
[Mh] Termos MeSH secundário: Animais
Carbocisteína/sangue
Carbocisteína/farmacocinética
Feminino
Masculino
Camundongos
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
70FD1KFU70 (Sulfur); 740J2QX53R (Carbocysteine); EC 1.14.16.1 (Phenylalanine Hydroxylase); S88TT14065 (Oxygen)
[Em] Mês de entrada:1610
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150905
[St] Status:MEDLINE
[do] DOI:10.3109/00498254.2015.1075259


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[PMID]:26170140
[Au] Autor:Guerra EN; Acevedo AC; Leite AF; Gozal D; Chardin H; De Luca Canto G
[Ad] Endereço:Department of Dentistry, Oral Histopathology Laboratory, Health Sciences Faculty, University of Brasília, Brasília, Brazil. Electronic address: elieteneves@unb.br.
[Ti] Título:Diagnostic capability of salivary biomarkers in the assessment of head and neck cancer: A systematic review and meta-analysis.
[So] Source:Oral Oncol;51(9):805-18, 2015 Sep.
[Is] ISSN:1879-0593
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The purpose of this systematic review and meta-analysis was to evaluate the diagnostic value of salivary biological markers in the diagnosis of head and neck carcinoma. Studies were gathered by searching Cochrane, EMBASE, LILACS, MEDLINE, and PubMed. The references were also crosschecked and a partial grey literature search was undertaken using Google Scholar. The methodology of selected studies was evaluated using the 14-item Quality Assessment Tool for Diagnostic Accuracy Studies. After a two-step selection process, 15 articles were identified and subjected to qualitative and quantitative analyses. The studies were homogeneous, and all had high methodological quality. Combined biomarkers demonstrated better accuracy with higher sensitivity and specificity than those tested individually. Furthermore, the salivary biomarkers reviewed predicted the early stages of head and neck carcinoma better than the advanced stages. A restricted set of five single biomarkers (interleukin-8, choline, pipecolinic acid, l-phenylalanine, and S-carboxymethyl-l-cysteine) as well as combined biomarkers demonstrated excellent diagnostic test accuracy. The present systematic review confirms the potential value of a selected set of salivary biomarkers as diagnostic tools for head and neck carcinoma.
[Mh] Termos MeSH primário: Biomarcadores/análise
Neoplasias de Cabeça e Pescoço/diagnóstico
Saliva/química
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Carbocisteína/análise
Colina/análise
Neoplasias de Cabeça e Pescoço/metabolismo
Seres Humanos
Interleucina-8/análise
Meia-Idade
Fenilalanina/análise
Piperidinas/análise
Sensibilidade e Especificidade
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS; REVIEW
[Nm] Nome de substância:
0 (Biomarkers); 0 (Interleukin-8); 0 (Piperidines); 47E5O17Y3R (Phenylalanine); 740J2QX53R (Carbocysteine); N91BDP6H0X (Choline)
[Em] Mês de entrada:1605
[Cu] Atualização por classe:150811
[Lr] Data última revisão:
150811
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150715
[St] Status:MEDLINE


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[PMID]:26159351
[Au] Autor:Fanigliulo A; De Filippis P; Curcuruto O; Repeto P; Roveda D; Hartenstein M; Adams E; Cabooter D
[Ad] Endereço:Aptuit, via Fleming 4, 37138 Verona, Italy.
[Ti] Título:Development and validation of a stability indicating method for S-carboxymethyl-L-cysteine and related degradation products in oral syrup formulation.
[So] Source:J Pharm Biomed Anal;115:39-47, 2015 Nov 10.
[Is] ISSN:1873-264X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:A stability-indicating method for the determination of S-carboxymethyl-L-cysteine and related degradation impurities in Exputex® 250mg/5mL syrup was developed in anion-exchange liquid chromatography mode. A forced degradation study supported the method development to ensure stability indicating conditions. Aqueous solutions of the active pharmaceutical ingredient and syrup samples at different pH-values were stress-tested in different thermal, light exposure and headspace conditions. One degradation product was detected in thermal stress studies at 60°C and 80°C in the pH range 5.0-7.0 and was identified by mass spectrometry as 5-oxo-thiomorpholine-3-carboxylic acid (lactam of carbocysteine). A second degradation product was only generated in moderately strong oxidizing conditions (0.5% H2O2 aqueous solution) and was identified as S-carboxymethyl-L-cysteine-(R/S)-sulphoxide (carbocysteine sulphoxide). The method was developed on a Zorbax SAX column, in isocratic mode. The mobile phase consisted of 200mM phosphate solution at pH 4.0 and acetonitrile (50:50 v/v) and UV detection was performed at a wavelength of 205nm. The method was linear for carbocysteine (R>0.9982) over a concentration range of 2.5-50µg/mL and 0.4-0.6mg/mL. Linearity for the impurities was shown from the LOQ to 50µg/mL. Specificity was verified and accuracy demonstrated for the active ingredient and its degradation products in syrup samples at 3 levels around their respective specification limits. Repeatability, intermediate precision and inter-laboratory reproducibility were assessed on three commercial batches, analyzed in triplicate by two operators at both the transferring and the receiving site and demonstrated a successful method transfer to the manufacturing quality control laboratory.
[Mh] Termos MeSH primário: Carbocisteína/análogos & derivados
Cromatografia Líquida de Alta Pressão/métodos
Expectorantes/análise
Lactamas/análise
Espectrometria de Massas por Ionização por Electrospray/métodos
[Mh] Termos MeSH secundário: Administração Oral
Carbocisteína/análise
Química Farmacêutica
Formas de Dosagem
Contaminação de Medicamentos
Estabilidade de Medicamentos
Estrutura Molecular
Reprodutibilidade dos Testes
Sensibilidade e Especificidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Dosage Forms); 0 (Expectorants); 0 (Lactams); 5439-87-2 (carbocysteine sulfoxide); 740J2QX53R (Carbocysteine)
[Em] Mês de entrada:1606
[Cu] Atualização por classe:150921
[Lr] Data última revisão:
150921
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150711
[St] Status:MEDLINE


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[PMID]:26126534
[Au] Autor:Shinya T; Yokota T; Nakayama S; Oki S; Mutoh J; Takahashi S; Sato K
[Ad] Endereço:Department of Clinical Biochemistry (T.S.,T.Y., S.N., S.O., K.S.) and Second Department of Pharmacology (J.M.), School of Pharmaceutical Science, Kyushu University of Health and Welfare, Nobeoka, Miyazaki, Japan; and Department of Immunobiology, School of Pharmacy and Pharmaceutical Science, Mukogaw
[Ti] Título:Orally Administered Mucolytic Drug l-Carbocisteine Inhibits Angiogenesis and Tumor Growth in Mice.
[So] Source:J Pharmacol Exp Ther;354(3):269-78, 2015 Sep.
[Is] ISSN:1521-0103
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Angiogenesis, the formation of new blood vessels from pre-existing vessels, is essential for the growth and metastasis of tumors. In this study, we found that l-carbocisteine, a widely used expectorant, potently inhibits angiogenesis in vitro and in vivo. An in vivo Matrigel plug assay revealed that l-carbocisteine (2.5 mg/kg i.p. twice daily) significantly inhibited vascular endothelial growth factor (VEGF)-induced angiogenesis. l-Carbocisteine also suppressed VEGF-stimulated proliferation, migration, and formation of capillary-like structures of human umbilical vein endothelial cells (HUVECs). We examined the signaling pathways affected in VEGF-stimulated HUVECs, and found that l-carbocisteine significantly inhibited VEGF-induced phosphorylation of phospholipase C (PLC) γ, protein kinase C (PKC) µ, and extracellular signal-related kinases (ERK) 1/2, which have been shown to be essential for angiogenesis. However, these inhibitory effects of l-carbocisteine were not observed in the HeLa human cervical cancer cell line. An in vivo study of Colon-26 tumor-bearing mice found that tumor volumes were significantly smaller in mice treated with l-carbocisteine (150 mg/kg administered orally twice daily) in comparison with vehicle-treated mice. However, l-carbocisteine had no direct effect on Colon-26 cell proliferation or ERK activation. Collectively, our results suggest that l-carbocisteine inhibits tumor angiogenesis by suppressing PLCγ/PKC/ERK signaling.
[Mh] Termos MeSH primário: Inibidores da Angiogênese/farmacologia
Carbocisteína/farmacologia
Proliferação Celular/efeitos dos fármacos
Neovascularização Patológica/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Linhagem Celular Tumoral
Movimento Celular/efeitos dos fármacos
Expectorantes/farmacologia
Células HeLa
Células Endoteliais da Veia Umbilical Humana/efeitos dos fármacos
Células Endoteliais da Veia Umbilical Humana/metabolismo
Seres Humanos
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Endogâmicos C57BL
Neovascularização Patológica/metabolismo
Fosfolipase C gama/metabolismo
Fosforilação/efeitos dos fármacos
Proteína Quinase C/metabolismo
Transdução de Sinais/efeitos dos fármacos
Fator A de Crescimento do Endotélio Vascular/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Angiogenesis Inhibitors); 0 (Expectorants); 0 (Vascular Endothelial Growth Factor A); 740J2QX53R (Carbocysteine); EC 2.7.10.- (protein kinase D); EC 2.7.11.13 (Protein Kinase C); EC 3.1.4.3 (Phospholipase C gamma)
[Em] Mês de entrada:1510
[Cu] Atualização por classe:150725
[Lr] Data última revisão:
150725
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150702
[St] Status:MEDLINE
[do] DOI:10.1124/jpet.115.224816



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