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[PMID]:29278707
[Au] Autor:Nguyen G; Park SY; Le CT; Park WS; Choi DH; Cho EH
[Ad] Endereço:Department of Internal Medicine, School of Medicine, Kangwon National University, Republic of Korea.
[Ti] Título:Metformin ameliorates activation of hepatic stellate cells and hepatic fibrosis by succinate and GPR91 inhibition.
[So] Source:Biochem Biophys Res Commun;495(4):2649-2656, 2018 01 22.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Chronic liver disease is becoming a major cause of morbidity and mortality worldwide. During liver injury, hepatic stellate cells (HSCs) trans-differentiate into activated myofibroblasts, which produce extracellular matrix. Succinate and succinate receptor (G-protein coupled receptor91, GPR91) signaling pathway has now emerged as a regulator of metabolic signaling. A previous study showed that succinate and its specific receptor, GPR91, are involved in the activation of HSCs and the overexpression of α-smooth muscle actin (α-SMA). Metformin, a well-known anti-diabetic drug, inhibits hepatic gluconeogenesis in the liver. Many studies have shown that metformin not only prevented, but also reversed, steatosis and inflammation in a nonalcoholic steatohepatitis (NASH) animal model. However, the role of metformin in HSC activation and succinate-GPR91 signaling has not been clarified. METHODS: The immortalized human HSCs, LX-2 cells, were used for the in vitro study. For the in vivo study, male C57BL/J6 mice were randomly divided into 3 groups and were fed with a methionine-choline-deficient diet (MCD diet group) as a nonalcoholic steatohepatitis (NASH) mouse model with or without 0.1% metformin for 12 weeks, or were fed a control methionine-choline-sufficient diet (MCS diet group). RESULTS: In our study, metformin and 5-aminoimidazole-4-carboxamide 1-ß-d-ribofuranoside (AICAR), which is an analog of adenosine monophosphate, were shown to suppress α-SMA expression via enhanced phosphorylation of AMP-activated protein kinase (AMPK) and inhibition of succinate-GPR91 signaling in activated LX-2 cells induced by palmitate- or succinate. Metformin and AICAR also reduced succinate concentration in the cell lysates when LX-2 cells were treated with palmitate. Moreover, metformin and AICAR reduced interleukin-6 and, transforming growth factor-ß1 production in succinate-treated LX-2 cells. Both metformin and AICAR inhibited succinate-stimulated HSC proliferation and cell migration. Mice fed a MCD diet demonstrated increased steatohepatitis and liver fibrosis compared to that of mice fed control diet. Metformin ameliorated steatohepatitis, liver fibrosis, inflammatory cytokine production and decreased α -SMA and GPR91expression in the livers of the MCD diet-fed mice. CONCLUSION: This study shows that metformin can attenuate activation of HSCs by activating the AMPK pathway and inhibiting the succinate-GPR91 pathway. Metformin has therapeutic potential for treating steatohepatitis and liver fibrosis.
[Mh] Termos MeSH primário: Células Estreladas do Fígado/efeitos dos fármacos
Células Estreladas do Fígado/metabolismo
Cirrose Hepática/tratamento farmacológico
Cirrose Hepática/metabolismo
Metformina/administração & dosagem
Receptores Acoplados a Proteínas-G/metabolismo
Ácido Succínico/metabolismo
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Relação Dose-Resposta a Droga
Regulação para Baixo/efeitos dos fármacos
Células Estreladas do Fígado/patologia
Seres Humanos
Hipoglicemiantes/administração & dosagem
Cirrose Hepática/patologia
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (GPR91 protein, mouse); 0 (Hypoglycemic Agents); 0 (Receptors, G-Protein-Coupled); 9100L32L2N (Metformin); AB6MNQ6J6L (Succinic Acid)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171227
[St] Status:MEDLINE


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[PMID]:29381705
[Au] Autor:Nag A; St John PC; Crowley MF; Bomble YJ
[Ad] Endereço:Computational Science Center, National Renewable Energy Laboratory, Golden, Colorado, United States of America.
[Ti] Título:Prediction of reaction knockouts to maximize succinate production by Actinobacillus succinogenes.
[So] Source:PLoS One;13(1):e0189144, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Succinate is a precursor of multiple commodity chemicals and bio-based succinate production is an active area of industrial bioengineering research. One of the most important microbial strains for bio-based production of succinate is the capnophilic gram-negative bacterium Actinobacillus succinogenes, which naturally produces succinate by a mixed-acid fermentative pathway. To engineer A. succinogenes to improve succinate yields during mixed acid fermentation, it is important to have a detailed understanding of the metabolic flux distribution in A. succinogenes when grown in suitable media. To this end, we have developed a detailed stoichiometric model of the A. succinogenes central metabolism that includes the biosynthetic pathways for the main components of biomass-namely glycogen, amino acids, DNA, RNA, lipids and UDP-N-Acetyl-α-D-glucosamine. We have validated our model by comparing model predictions generated via flux balance analysis with experimental results on mixed acid fermentation. Moreover, we have used the model to predict single and double reaction knockouts to maximize succinate production while maintaining growth viability. According to our model, succinate production can be maximized by knocking out either of the reactions catalyzed by the PTA (phosphate acetyltransferase) and ACK (acetyl kinase) enzymes, whereas the double knockouts of PEPCK (phosphoenolpyruvate carboxykinase) and PTA or PEPCK and ACK enzymes are the most effective in increasing succinate production.
[Mh] Termos MeSH primário: Actinobacillus/metabolismo
Técnicas de Silenciamento de Genes
Ácido Succínico/metabolismo
[Mh] Termos MeSH secundário: Actinobacillus/enzimologia
Actinobacillus/genética
Biomassa
Meios de Cultura
Fermentação
Modelos Biológicos
Fosfato Acetiltransferase/genética
Fosfato Acetiltransferase/metabolismo
Fosfoenolpiruvato Carboxiquinase (ATP)/genética
Fosfoenolpiruvato Carboxiquinase (ATP)/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Culture Media); AB6MNQ6J6L (Succinic Acid); EC 2.3.1.8 (Phosphate Acetyltransferase); EC 4.1.1.49 (Phosphoenolpyruvate Carboxykinase (ATP))
[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:180131
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189144


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[PMID]:29366478
[Au] Autor:Park SY; Le CT; Sung KY; Choi DH; Cho EH
[Ad] Endereço:Department of Internal Medicine, School of Medicine, Kangwon National University, Republic of Korea.
[Ti] Título:Succinate induces hepatic fibrogenesis by promoting activation, proliferation, and migration, and inhibiting apoptosis of hepatic stellate cells.
[So] Source:Biochem Biophys Res Commun;496(2):673-678, 2018 02 05.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Liver fibrosis is a progressive pathological process that accompanies wound healing; however, therapeutics for reversing hepatic fibrosis are unavailable. Activation of hepatic stellate cells (HSCs) play a critical role in liver fibrosis. Recent reports showed that succinate and its receptor, G-protein coupled receptor 91 (GPR91), act as signaling molecules during the activation of HSCs. However, the role of succinate in proliferation, apoptosis, and migration of HSCs has not been studied. In this study, we determined whether succinate regulates proliferation, apoptosis, and migration of HSCs and induces liver fibrosis in a mouse model. Succinate treatment not only induced activation of HSCs, but also increased the proliferation and migration of LX-2 HSCs and inhibited apoptosis. To investigate whether succinate causes hepatic fibrosis, 100 mg/kg succinate or control PBS was administered by intraperitoneal injection to mice once a day for four weeks. There were significant molecular changes such as increased α-SMA and collagen type 1 production and increased production of inflammatory cytokines such as IL-6 and TNF-α, but not TGF-ß, in the succinate-treated group compared to the control group. However, no morphological changes were observed in Masson's trichrome staining. In conclusion, the present study demonstrated that succinate induces activation, proliferation, and migration of HSCs and attenuates apoptosis in LX-2 HSCs. Therefore, inhibition of succinate accumulation may be an effective method for reversing liver fibrosis by controlling HSC survival and growth.
[Mh] Termos MeSH primário: Células Estreladas do Fígado/patologia
Cirrose Hepática/metabolismo
Fígado/patologia
Ácido Succínico/metabolismo
[Mh] Termos MeSH secundário: Actinas/análise
Actinas/metabolismo
Animais
Apoptose
Linhagem Celular
Movimento Celular
Proliferação Celular
Células Estreladas do Fígado/citologia
Células Estreladas do Fígado/metabolismo
Seres Humanos
Fígado/citologia
Fígado/metabolismo
Cirrose Hepática/patologia
Masculino
Camundongos Endogâmicos C57BL
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Actins); 0 (alpha-smooth muscle actin, mouse); AB6MNQ6J6L (Succinic Acid)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180216
[Lr] Data última revisão:
180216
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180126
[St] Status:MEDLINE


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[PMID]:29364609
[Ti] Título:[Not Available.]
[So] Source:Mikrobiologiia;85(5):613-616, 2016 Sep.
[Is] ISSN:0026-3656
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Mh] Termos MeSH primário: Actinobacteria/metabolismo
Caprolactama/análogos & derivados
Caprolactama/metabolismo
Polímeros/metabolismo
[Mh] Termos MeSH secundário: Acetilcoenzima A/metabolismo
Actinobacteria/isolamento & purificação
Adipatos/metabolismo
Ácido Aminocaproico/metabolismo
Caproatos/metabolismo
Meios de Cultura/química
Hidrólise
Esgotos/microbiologia
Ácido Succínico/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (6-oxohexanoic acid); 0 (Adipates); 0 (Caproates); 0 (Culture Media); 0 (Polymers); 0 (Sewage); 25038-54-4 (nylon 6); 6879X594Z8 (Caprolactam); 72-89-9 (Acetyl Coenzyme A); 76A0JE0FKJ (adipic acid); AB6MNQ6J6L (Succinic Acid); U6F3787206 (Aminocaproic Acid)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180208
[Lr] Data última revisão:
180208
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180125
[St] Status:MEDLINE


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[PMID]:28463479
[Au] Autor:Hong CY; Ryu SH; Jeong H; Lee SS; Kim M; Choi IG
[Ad] Endereço:Division of Wood Chemistry & Microbiology, Department of Forest Products, National Institute of Forest Science , Seoul, Republic of Korea.
[Ti] Título:Phanerochaete chrysosporium Multienzyme Catabolic System for in Vivo Modification of Synthetic Lignin to Succinic Acid.
[So] Source:ACS Chem Biol;12(7):1749-1759, 2017 Jul 21.
[Is] ISSN:1554-8937
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Whole cells of the basidiomycete fungus Phanerochaete chrysosporium (ATCC 20696) were applied to induce the biomodification of lignin in an in vivo system. Our results indicated that P. chrysosporium has a catabolic system that induces characteristic biomodifications of synthetic lignin through a series of redox reactions, leading not only to the degradation of lignin but also to its polymerization. The reducing agents ascorbic acid and α-tocopherol were used to stabilize the free radicals generated from the ligninolytic process. The application of P. chrysosporium in combination with reducing agents produced aromatic compounds and succinic acid as well as degraded lignin polymers. P. chrysosporium selectively catalyzed the conversion of lignin to succinic acid, which has an economic value. A transcriptomic analysis of P. chrysosporium suggested that the bond cleavage of synthetic lignin was caused by numerous enzymes, including extracellular enzymes such as lignin peroxidase and manganese peroxidase, and that the aromatic compounds released were metabolized in both the short-cut and classical tricarboxylic acid cycles of P. chrysosporium. In conclusion, P. chrysosporium is suitable as a biocatalyst for lignin degradation to produce a value-added product.
[Mh] Termos MeSH primário: Lignina/metabolismo
Complexos Multienzimáticos/química
Phanerochaete/enzimologia
Ácido Succínico/síntese química
[Mh] Termos MeSH secundário: Ácido Ascórbico/química
Radicais Livres
Lignina/química
Peso Molecular
Nitrobenzenos/química
Oxirredução
Phanerochaete/metabolismo
Ácido Succínico/química
Ácido Succínico/metabolismo
Tocoferóis/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Free Radicals); 0 (Multienzyme Complexes); 0 (Nitrobenzenes); 9005-53-2 (Lignin); AB6MNQ6J6L (Succinic Acid); E57JCN6SSY (nitrobenzene); PQ6CK8PD0R (Ascorbic Acid); R0ZB2556P8 (Tocopherols)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180207
[Lr] Data última revisão:
180207
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.1021/acschembio.7b00046


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[PMID]:28450394
[Au] Autor:Korge P; John SA; Calmettes G; Weiss JN
[Ad] Endereço:From the UCLA Cardiovascular Research Laboratory and the Departments of Medicine (Cardiology) and Physiology, David Geffen School of Medicine at UCLA, Los Angeles, California 90095.
[Ti] Título:Reactive oxygen species production induced by pore opening in cardiac mitochondria: The role of complex II.
[So] Source:J Biol Chem;292(24):9896-9905, 2017 06 16.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Succinate-driven reverse electron transport (RET) through complex I is hypothesized to be a major source of reactive oxygen species (ROS) that induces permeability transition pore (PTP) opening and damages the heart during ischemia/reperfusion. Because RET can only generate ROS when mitochondria are fully polarized, this mechanism is self-limiting once PTP opens during reperfusion. In the accompanying article (Korge, P., Calmettes, G., John, S. A., and Weiss, J. N. (2017) 292, 9882-9895), we showed that ROS production after PTP opening can be sustained when complex III is damaged (simulated by antimycin). Here we show that complex II can also contribute to sustained ROS production in isolated rabbit cardiac mitochondria following inner membrane pore formation induced by either alamethicin or calcium-induced PTP opening. Two conditions are required to maximize malonate-sensitive ROS production by complex II in isolated mitochondria: ( ) complex II inhibition by atpenin A5 or complex III inhibition by stigmatellin that results in succinate-dependent reduction of the dicarboxylate-binding site of complex II (site II ); ( ) pore opening in the inner membrane resulting in rapid efflux of succinate/fumarate and other dicarboxylates capable of competitively binding to site II The decrease in matrix [dicarboxylate] allows O access to reduced site II , thereby making electron donation to O possible, explaining the rapid increase in ROS production provided that site II is reduced. Because ischemia is known to inhibit complexes II and III and increase matrix succinate/fumarate levels, we hypothesize that by allowing dicarboxylate efflux from the matrix, PTP opening during reperfusion may activate sustained ROS production by this mechanism after RET-driven ROS production has ceased.
[Mh] Termos MeSH primário: Complexo II de Transporte de Elétrons/metabolismo
Mitocôndrias Cardíacas/metabolismo
Modelos Moleculares
Espécies Reativas de Oxigênio/agonistas
[Mh] Termos MeSH secundário: Alameticina/farmacologia
Animais
Sítios de Ligação
Ligação Competitiva
Biocatálise/efeitos dos fármacos
Sinalização do Cálcio/efeitos dos fármacos
Transporte de Elétrons/efeitos dos fármacos
Complexo II de Transporte de Elétrons/antagonistas & inibidores
Complexo II de Transporte de Elétrons/química
Inibidores Enzimáticos/farmacologia
Fumaratos/metabolismo
Ionóforos/farmacologia
Potencial da Membrana Mitocondrial/efeitos dos fármacos
Mitocôndrias Cardíacas/química
Mitocôndrias Cardíacas/efeitos dos fármacos
Oxirredução
Permeabilidade/efeitos dos fármacos
Polienos/farmacologia
Porosidade
Piridonas/farmacologia
Coelhos
Espécies Reativas de Oxigênio/metabolismo
Ácido Succínico/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Enzyme Inhibitors); 0 (Fumarates); 0 (Ionophores); 0 (Polyenes); 0 (Pyridones); 0 (Reactive Oxygen Species); 119509-24-9 (atpenin A5); 27061-78-5 (Alamethicin); 91682-96-1 (stigmatellin); AB6MNQ6J6L (Succinic Acid); EC 1.3.5.1 (Electron Transport Complex II)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:180205
[Lr] Data última revisão:
180205
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M116.768325


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[PMID]:29211771
[Au] Autor:Ferro A; Carbone E; Zhang J; Marzouk E; Villegas M; Siegel A; Nguyen D; Possidente T; Hartman J; Polley K; Ingram MA; Berry G; Reynolds TH; Possidente B; Frederick K; Ives S; Lagalwar S
[Ad] Endereço:Neuroscience Program, Skidmore College, Saratoga Springs, New York, United States of America.
[Ti] Título:Short-term succinic acid treatment mitigates cerebellar mitochondrial OXPHOS dysfunction, neurodegeneration and ataxia in a Purkinje-specific spinocerebellar ataxia type 1 (SCA1) mouse model.
[So] Source:PLoS One;12(12):e0188425, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mitochondrial dysfunction plays a significant role in neurodegenerative disease including ataxias and other movement disorders, particularly those marked by progressive degeneration in the cerebellum. In this study, we investigate the role of mitochondrial oxidative phosphorylation (OXPHOS) deficits in cerebellar tissue of a Purkinje cell-driven spinocerebellar ataxia type 1 (SCA1) mouse. Using RNA sequencing transcriptomics, OXPHOS complex assembly analysis and oxygen consumption assays, we report that in the presence of mutant polyglutamine-expanded ataxin-1, SCA1 mice display deficits in cerebellar OXPHOS complex I (NADH-coenzyme Q oxidoreductase). Complex I genes are upregulated at the time of symptom onset and upregulation persists into late stage disease; yet, functional assembly of complex I macromolecules are diminished and oxygen respiration through complex I is reduced. Acute treatment of postsymptomatic SCA1 mice with succinic acid, a complex II (succinate dehydrogenase) electron donor to bypass complex I dysfunction, ameliorated cerebellar OXPHOS dysfunction, reduced cerebellar pathology and improved motor behavior. Thus, exploration of mitochondrial dysfunction and its role in neurodegenerative ataxias, and warrants further investigation.
[Mh] Termos MeSH primário: Cerebelo/metabolismo
Modelos Animais de Doenças
Mitocôndrias/metabolismo
Células de Purkinje/patologia
Ataxias Espinocerebelares/metabolismo
Ácido Succínico/administração & dosagem
[Mh] Termos MeSH secundário: Animais
Camundongos
Camundongos Transgênicos
Fosforilação Oxidativa
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
AB6MNQ6J6L (Succinic Acid)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171229
[Lr] Data última revisão:
171229
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171207
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188425


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[PMID]:28465086
[Au] Autor:Du Y; Zhang W; He R; Ismail M; Ling L; Yao C; Fu Z; Li X
[Ad] Endereço:School of Chemistry and Chemical Engineering, Southeast University, Nanjing 211189, PR China.
[Ti] Título:Dual 7-ethyl-10-hydroxycamptothecin conjugated phospholipid prodrug assembled liposomes with in vitro anticancer effects.
[So] Source:Bioorg Med Chem;25(12):3247-3258, 2017 06 15.
[Is] ISSN:1464-3391
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:7-Ethyl-10-hydroxycamptothecin (SN38), as a highly active topoisomerase I inhibitor, is 200-2000-fold more cytotoxic than irinotecan (CPT-11) commercially available as Camptosar®. However, poor solubility and low stability extensively restricted its clinical utility. In this report, dual SN38 phospholipid conjugate (Di-SN38-PC) prodrug based liposomes were developed in order to compact these drawbacks. Di-SN38-PC prodrug was first synthesized by inhomogeneous conjugation of two SN38-20-O-succinic acid molecules with L-α-glycerophosphorylcholine (GPC). The assembly of the prodrug was carried out without any excipient by using thin film method. Dynamic light scattering (DLS), transmission electron microscope (TEM) and cryogenic transmission electron microscopy (cyro-TEM) characterization indicated that Di-SN38-PC can form spherical liposomes with narrow particle size (<200nm) and negatively charged surface (-21.6±3.5mV). The loading efficiency of SN38 is 65.2 wt.% after a simple calculation. In vitro release test was further performed in detail. The results demonstrated that Di-SN38-PC liposomes were stable in neutral environment but degraded in a weakly acidic condition thereby released parent drug SN38 effectively. Cellular uptake studies reflected that the liposomes could be internalized into cells more significantly than SN38. In vitro antitumor activities were finally evaluated by MTT assay, colony formation assay, flow cytometry, RT-PCR analysis and Western Blot. The results showed that Di-SN38-PC liposomes had a comparable cytotoxicity with SN38 against MCF-7 and HBL-100, and a selective promotion of apoptosis of tumor cells. Furthermore, a pharmacokinetics test showed that Di-SN38-PC liposomes had a longer circulating time in blood compared with the parent drug. All the results indicate that Di-SN38-PC liposomes are an effective delivery system of SN38.
[Mh] Termos MeSH primário: Antineoplásicos Fitogênicos/química
Antineoplásicos Fitogênicos/farmacologia
Camptotecina/análogos & derivados
Pró-Fármacos/química
Pró-Fármacos/farmacologia
[Mh] Termos MeSH secundário: Animais
Antineoplásicos Fitogênicos/administração & dosagem
Antineoplásicos Fitogênicos/farmacocinética
Camptotecina/administração & dosagem
Camptotecina/química
Camptotecina/farmacocinética
Camptotecina/farmacologia
Linhagem Celular Tumoral
Sobrevivência Celular/efeitos dos fármacos
Seres Humanos
Lipossomos
Camundongos Endogâmicos BALB C
Camundongos Nus
Neoplasias/tratamento farmacológico
Neoplasias/metabolismo
Fosfolipídeos/administração & dosagem
Fosfolipídeos/química
Fosfolipídeos/farmacocinética
Fosfolipídeos/farmacologia
Pró-Fármacos/administração & dosagem
Pró-Fármacos/farmacocinética
Solubilidade
Ácido Succínico/administração & dosagem
Ácido Succínico/química
Ácido Succínico/farmacocinética
Ácido Succínico/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antineoplastic Agents, Phytogenic); 0 (Liposomes); 0 (Phospholipids); 0 (Prodrugs); 9Z01632KRV (10-hydroxycamptothecin); AB6MNQ6J6L (Succinic Acid); XT3Z54Z28A (Camptothecin)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171208
[Lr] Data última revisão:
171208
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE


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[PMID]:28461222
[Au] Autor:Jørgensen LB; MacMillan HA; Overgaard J
[Ad] Endereço:Zoophysiology, Department of Bioscience, Aarhus University, C.F. Møllers Allé 3, Building 1131, 8000 Aarhus C, Denmark. Electronic address: lisa.b.joergensen@gmail.com.
[Ti] Título:Cold mortality is not caused by oxygen limitation or loss of ion homeostasis in the tropical freshwater shrimp Macrobrachium rosenbergii.
[So] Source:Cryobiology;76:146-149, 2017 Jun.
[Is] ISSN:1090-2392
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Using the tropical crustacean Macrobrachium rosenbergii we investigate two popular hypotheses proposed to explain loss of function in ectotherms exposed to critically high and low temperatures. Specifically, we examine whether acute cold stress disrupts hemolymph and muscle ion balance or causes a loss of oxygen availability. We found that acute cold stress causes loss of righting response at 13 °C, but that a cold-induced loss of ion-balance only occurs after onset of mortality. In regards to oxygen availability, we found no decrease in hemolymph oxygen content during cold exposure, and no changes in the concentrations of the anaerobic end products l-lactate and succinate in the tail muscle of the shrimp. Therefore, our results support neither of these two popular hypotheses and it remains unknown what physiological perturbations determine the lower limits of thermal tolerance in Macrobrachium rosenbergii.
[Mh] Termos MeSH primário: Temperatura Baixa/efeitos adversos
Palaemonidae/metabolismo
[Mh] Termos MeSH secundário: Animais
Hemolinfa/metabolismo
Homeostase
Ácido Láctico/metabolismo
Músculos/metabolismo
Oxigênio/metabolismo
Ácido Succínico/metabolismo
Equilíbrio Hidroeletrolítico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
33X04XA5AT (Lactic Acid); AB6MNQ6J6L (Succinic Acid); S88TT14065 (Oxygen)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE


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[PMID]:28926680
[Au] Autor:Ahn JH; Bang J; Kim WJ; Lee SY
[Ad] Endereço:Metabolic and Biomolecular Engineering National Research Laboratory, Department of Chemical and Biomolecular Engineering (BK21 Plus program), BioProcess Engineering Research Center, Institute for the BioCentury, Yuseong-gu, Daejeon, Republic of Korea.
[Ti] Título:Formic acid as a secondary substrate for succinic acid production by metabolically engineered Mannheimia succiniciproducens.
[So] Source:Biotechnol Bioeng;114(12):2837-2847, 2017 Dec.
[Is] ISSN:1097-0290
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:There has been much effort exerted to reduce one carbon (C1) gas emission to address climate change. As one promising way to more conveniently utilize C1 gas, several technologies have been developed to convert C1 gas into useful chemicals such as formic acid (FA). In this study, systems metabolic engineering was utilized to engineer Mannheimia succiniciproducens to efficiently utilize FA. C isotope analysis of M. succiniciproducens showed that FA could be utilized through formate dehydrogenase (FDH) reaction and/or the reverse reaction of pyruvate formate lyase (PFL). However, the naturally favored forward reaction of PFL was found to lower the SA yield from FA. In addition, FA assimilation via FDH was found to be more efficient than the reverse reaction of PFL. Thus, the M. succiniciproducens LPK7 strain, which lacks in pfl, ldh, pta, and ack genes, was selected as a base strain. In silico metabolic analysis confirmed that utilization of FA would be beneficial for the enhanced production of SA and suggested FDH as an amplification target. To find a suitable FDH, four different FDHs from M. succiniciproducens, Methylobacterium extorquens, and Candida boidinii were amplified in LPK7 strain to enhance FA assimilation. High-inoculum density cultivation using C labeled sodium formate was performed to evaluate FA assimilation efficiency. Fed-batch fermentations of the LPK7 (pMS3-fdh2 meq) strain was carried out using glucose, sucrose, or glycerol as a primary carbon source and FA as a secondary carbon source. As a result, this strain produced 76.11 g/L SA with the yield and productivity of 1.28 mol/mol and 4.08 g/L/h, respectively, using sucrose and FA as dual carbon sources. The strategy employed here will be similarly applicable in developing microorganisms to utilize FA and to produce valuable chemicals and materials from FA.
[Mh] Termos MeSH primário: Formiato Desidrogenases/genética
Formiatos/metabolismo
Melhoramento Genético/métodos
Mannheimia/fisiologia
Engenharia Metabólica/métodos
Análise do Fluxo Metabólico/métodos
Ácido Succínico/metabolismo
[Mh] Termos MeSH secundário: Simulação por Computador
Mannheimia/classificação
Modelos Biológicos
Especificidade da Espécie
Especificidade por Substrato
Ácido Succínico/isolamento & purificação
Regulação para Cima/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Formates); 0YIW783RG1 (formic acid); AB6MNQ6J6L (Succinic Acid); EC 1.2.1.2 (Formate Dehydrogenases)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171113
[Lr] Data última revisão:
171113
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170920
[St] Status:MEDLINE
[do] DOI:10.1002/bit.26435



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