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[PMID]: 29524843
[Au] Autor:Sena FV; Sousa FM; Oliveira ASF; Soares CM; Catarino T; Pereira MM
[Ad] Address:Instituto de Tecnologia Química e Biológica - António Xavier, Universidade Nova de Lisboa, Av. da Republica EAN, 2780-157 Oeiras, Portugal.
[Ti] Title:Regulation of the mechanism of Type-II NADH: Quinone oxidoreductase from S. aureus.
[So] Source:Redox Biol;16:209-214, 2018 Feb 17.
[Is] ISSN:2213-2317
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Type-II NADH:quinone oxidoreductases (NDH-2s) are membrane proteins involved in respiratory chains and the only enzymes with NADH:quinone oxidoreductase activity expressed in Staphylococcus aureus (S. aureus), one of the most common causes of clinical infections. NDH-2s are members of the two-Dinucleotide Binding Domains Flavoprotein (tDBDF) superfamily, having a flavin adenine dinucleotide, FAD, as prosthetic group and NAD(P)H as substrate. The establishment of a Charge-Transfer Complex (CTC) between the isoalloxazine ring of the reduced flavin and the nicotinamide ring of NAD+ in NDH-2 was described, and in this work we explored its role in the kinetic mechanism using different electron donors and electron acceptors. We observed that CTC slows down the rate of the second half reaction (quinone reduction) and determines the effect of HQNO, an inhibitor. Also, protonation equilibrium simulations clearly indicate that the protonation probability of an important residue for proton transfer to the active site (D302) is influenced by the presence of the CTC. We propose that CTC is critical for the overall mechanism of NDH-2 and possibly relevant to keep a low quinol/quinone ratio and avoid excessive ROS production in vivo.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

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[PMID]: 29524803
[Au] Autor:Del Cueto J; Møller BL; Dicenta F; Sánchez-Pérez R
[Ad] Address:Department of Plant Breeding, CEBAS-CSIC, P.O. Box 164, 30100 Campus Universitario de Espinardo, Murcia, Spain; University of Copenhagen, Faculty of Science, Plant Biochemistry Laboratory, DK-1871 Copenhagen C, Denmark; VILLUM Research Center for Plant Plasticity, DK-1871 Frederiksberg C, Denmark.
[Ti] Title:ß-Glucosidase activity in almond seeds.
[So] Source:Plant Physiol Biochem;126:163-172, 2017 Dec 16.
[Is] ISSN:1873-2690
[Cp] Country of publication:France
[La] Language:eng
[Ab] Abstract:Almond bitterness is the most important trait for breeding programs since bitter-kernelled seedlings are usually discarded. Amygdalin and its precursor prunasin are hydrolyzed by specific enzymes called ß-glucosidases. In order to better understand the genetic control of almond bitterness, some studies have shown differences in the location of prunasin hydrolases (PH, the ß-glucosidase that degrades prunasin) in sweet and bitter genotypes. The aim of this work was to isolate and characterize different PHs in sweet- and bitter-kernelled almonds to determine whether differences in their genomic or protein sequences are responsible for the sweet or bitter taste of their seeds. RNA was extracted from the tegument, nucellus and cotyledon of one sweet (Lauranne) and two bitter (D05-187 and S3067) almond genotypes throughout fruit ripening. Sequences of nine positive Phs were then obtained from all of the genotypes by RT-PCR and cloning. These clones, from mid ripening stage, were expressed in a heterologous system in tobacco plants by agroinfiltration. The PH activity was detected using the Feigl-Anger method and quantifying the hydrogen cyanide released with prunasin as substrate. Furthermore, ß-glucosidase activity was detected by Fast Blue BB salt and Umbelliferyl method. Differences at the sequence level (SNPs) and in the activity assays were detected, although no correlation with bitterness was found.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  3 / 458715 MEDLINE  
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[PMID]: 29524802
[Au] Autor:Ferreira PAA; Marchezan C; Ceretta CA; Tarouco CP; Lourenzi CR; Silva LS; Soriani HH; Nicoloso FT; Cesco S; Mimmo T; Brunetto G
[Ad] Address:Department of Soil Science, Federal University of Santa Maria, CEP 97105-900, Rio Grande do Sul, Brazil.
[Ti] Title:Soil amendment as a strategy for the growth of young vines when replanting vineyards in soils with high copper content.
[So] Source:Plant Physiol Biochem;126:152-162, 2018 Mar 02.
[Is] ISSN:1873-2690
[Cp] Country of publication:France
[La] Language:eng
[Ab] Abstract:Soil contamination with copper (Cu)-based agrochemicals used in vineyards for pest control is a growing problem. In this context, the application of soil amendment to limit Cu toxicity, especially for young plants after the replanting of vineyards, has been a concern for winemakers. Therefore, the aim of this study was to evaluate how different amendments can contribute to the decrease in Cu availability in areas vocated to viticulture. Furthermore, the aim was to evaluate to the effect of Cu on the biochemical and physiological changes in the development of the young vine plants, both at the shoot and the root level. Vine plants were grown in a greenhouse using a Typic Hapludalf soil characterized by 87.5 mg of Cu kg (control). Three different amendments were applied to the soil: limestone (3 Mg ha ), calcium silicate (3 Mg ha ) and vermicompost (30 g of C kg ). The amendment with vermicompost and calcium silicate caused a significant alkalization of the soil solution. Moreover, specifically for the treatment with vermicompost, the levels of Cu in the soil solution were consistently diminished with a clear benefit for plants (+89% biomass accumulation at the shoot level). In addition, this soil amendment led to a higher photosynthetic rate, lower superoxide dismutase (SOD, EC 1.15.1.1) and guaiacol peroxidase (POD, EC 1.11.1.7) activity and a higher percentage of fine roots with diameter between 0 < L ≥ 0.2 mm (particularly active in water and nutrient acquisition). In conclusion, results showed that vermicompost effectively reduced Cu phytotoxicityin young vines grown in soils with high Cu contents. Furthermore, this amendment might be an asset in enhancing the availability of other important micronutrients such as iron.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

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[PMID]: 29524564
[Au] Autor:Benabdelaziz I; Gómez-Ruiz S; Benkhaled M; Carralero S; Schenker P; Salm A; Gertsch J; Haba H
[Ad] Address:Laboratoire de Chimie et Chimie de l'Environnement (L.C.C.E.), Département de Chimie, Faculté des Sciences de la matière, Université de Batna-1, Batna 05000, Algeria; Departamento de Biología y Geología, Física y Química Inorgánica, E.S.C.E.T., Universidad Rey Juan Carlos, 28933 Móstoles, Madrid, Sp
[Ti] Title:New cycloartane-type ester triterpenes from Euphorbia pterococca and biological evaluation.
[So] Source:Fitoterapia;, 2018 Mar 07.
[Is] ISSN:1873-6971
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:From acetonic extract of the whole plant Euphorbia pterococca Brot. (Euphorbiaceae), four new cycloartane-type ester triterpenes named cycloartenyl-2'E,4'E-decadienoate (1), cycloartenyl-2'E,4'Z-decadienoate (2), 24-methylenecycloartanyl-2'E,4'Z-tetradecadienoate (3), and 24-oxo-29-norcycloartanyl-2'E,4'Z-hexadecadienoate (4) were obtained along with nine known tetracyclic triterpenes (5-13). Their structures were established mainly by extensive use of spectroscopic techniques, including 1D ( H and C) and 2D homo- and heteronuclear NMR experiments (COSY, HSQC, HMBC and NOESY), and mass spectrometry (HRESIMS), and by comparison with data reported in the literature. In addition, the new compounds 1-3 have been tested for cytotoxicity, trypanocidal effects and on enzymes involved in endocannabinoid degradation. While inactive in all assays up to 100 µM, 1 showed selective inhibition of α/ß-hydrolase 12 with an IC of 11.6 ±â€¯1.9 µM.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

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[PMID]: 29524558
[Au] Autor:Cao X; Zhou Y; Sun H; Xu M; Bi X; Zhao Z; Shen B; Wan F; Hong Z; Lan L; Luo L; Guo Z; Yin Z
[Ad] Address:Jiangsu Province Key Laboratory for Molecular and Medical Biotechnology, College of Life Science, Nanjing Normal University, Nanjing, 210046, Jiangsu, PR China.
[Ti] Title:EGFR-TKI-induced HSP70 degradation and BER suppression facilitate the occurrence of the EGFR T790 M resistant mutation in lung cancer cells.
[So] Source:Cancer Lett;, 2018 Mar 07.
[Is] ISSN:1872-7980
[Cp] Country of publication:Ireland
[La] Language:eng
[Ab] Abstract:Non-small cell lung cancer (NSCLC) patients harboring EGFR-activating mutations initially respond to EGFR tyrosine kinase inhibitors (EGFR-TKIs) and have shown favorable outcomes. However, acquired drug resistance to EGFR-TKIs develops in almost all patients mainly due to the EGFR T790 M mutation. Here, we show that treatment with low-dose EGFR-TKI results in the emergence of the EGFR T790 M mutation and in the reduction of HSP70 protein levels in HCC827 cells. Erlotinib treatment inhibits HSP70 phosphorylation at tyrosine 41 and increases HSP70 ubiquitination, resulting in HSP70 degradation. We show that EGFR-TKI treatment causes increased DNA damage and enhanced gene mutation rates, which are secondary to the EGFR-TKI-induced reduction of HSP70 protein. Importantly, HSP70 overexpression delays the occurrence of Erlotinib-induced EGFR T790 M mutation. We further demonstrate that HSP70 interacts with multiple enzymes in the base excision repair (BER) pathway and promotes not only the efficiency but also the fidelity of BER. Collectively, our findings show that EGFR-TKI treatment facilitates gene mutation and the emergence of EGFR T790 M secondary mutation by the attenuation of BER via induction of HSP70 protein degradation.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

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[PMID]: 29524495
[Au] Autor:Osman WHW; Lin MI; Kondo K; Nagata T; Katahira M
[Ad] Address:Graduate School of Energy Science, Kyoto University, Japan.
[Ti] Title:Characterization of the glutathione S-transferases that belong to the GSTFuA class in Ceriporiopsis subvermispora: Implications in intracellular detoxification and metabolism of wood-derived compounds.
[So] Source:Int J Biol Macromol;, 2018 Mar 07.
[Is] ISSN:1879-0003
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Glutathione S-transferases (GSTs) of wood-degrading fungi play essential roles in cellular detoxification processes and endogenous metabolism. Fungal GSTs of GSTFuA class are suggested to be involved in lignin degradation. Ceriporiopsis subvermispora is one of the important model fungi of the selective lignin degraders, we found it interesting to study its GSTs. Here, we characterized the activities of two GSTs of the GSTFuA class of C. subvermispora (CsGST63524 and CsGST83044). A high-yield expression systems involving Escherichia coli was developed for each of these enzymes. Both enzymes were found to exhibit GSH-conjugation activity toward 1-chloro-2,4-dinitrobenzene, and GSH-peroxidase activity toward cumene hydroperoxide. Both enzymes showed high GSH-conjugation activity under basic conditions (pH 8.0 to 9.0), and the optimum temperature for their activity was 40 °C. In addition, three fluorescent compounds were used i.e., methylumbelliferyl acetovanillone was used to monitor etherase activity, and 5-chloromethylfluorescein diacetate and 4-methylumbelliferyl acetate to monitor esterase activity. CsGST83044 exhibited both etherase and esterase activities, while CsGST63524 displayed only esterase activity, which was much higher than that of CsGST83044. These findings imply the functional diversity of the GSTFuA class GSTs of C. subvermispora, suggesting that each protein plays distinctive roles in both the fungal detoxification system and wood compound metabolism.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  7 / 458715 MEDLINE  
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[PMID]: 29524404
[Au] Autor:Zhai X; Zhang Z; Liu W; Liu B; Zhang R; Wang W; Zheng W; Xu F; Wang J; Chen Y
[Ad] Address:Department of Emergency Medicine and Chest Pain Center, Qilu Hospital, Shandong University, Jinan, China; Institute of Emergency and Critical Care Medicine, Shandong University, Jinan, China; Key Laboratory of Emergency and Critical Care Medicine of Shandong Province, Qilu Hospital, Shandong Univers
[Ti] Title:Protective effect of ALDH2 against cyclophosphamide-induced acute hepatotoxicity via attenuating oxidative stress and reactive aldehydes.
[So] Source:Biochem Biophys Res Commun;, 2018 Mar 07.
[Is] ISSN:1090-2104
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Cyclophosphamide (CY) is a widely used chemotherapeutic agent that is associated with severe side effects, such as hepatotoxicity and nephrotoxicity. However, the extent, mechanisms and potential prevention and treatment strategies of CY-induced acute hepatotoxicity and nephrotoxicity are largely unknown. In this study, we determined the existence and extent of CY-induced acute hepatotoxicity and nephrotoxicity, and demonstrated the effect of ALDH2 on CY-induced acute tissue toxicity and related mechanisms. Adult male C57BL/6J (wide-type, WT) and ALDH2 (KO) mice were divided into four groups: WT, WT + CY, KO + CY and WT + CY + Alda-1. Biochemical analysis showed that plasma ALT was increased by 35.8% in KO + CY group and decreased by 21.1% in WT + CY + Alda-1 group compared to WT + CY group (P < 0.05, respectively). However, there was no significant difference among WT, WT + CY and KO + CY groups regarding plasma renal marker enzymes, including blood urea nitrogen, creatinine and cystatin C. Levels of reactive oxygen species (ROS) and toxic aldehydes (acrolein, 4-hydroxynonenol and malondialdehyde) were increased significantly in KO + CY group and decreased significantly in WT + CY + Alda-1 group compared to WT + CY group (P < 0.05, respectively). These findings demonstrate that CY could induce acute hepatotoxicity without nephrotoxicity, and ALDH2 plays a protective role in CY-induced acute hepatotoxicity. The underlying mechanisms are associated with attenuating oxidative stress and detoxifying reactive aldehydes.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

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[PMID]: 29524384
[Au] Autor:Lasagni Vitar RM; Tau J; Janezic NS; Tesone AI; Hvozda Arana AG; Reides CG; Berra A; Ferreira SM; Llesuy SF
[Ad] Address:University of Buenos Aires, Faculty of Pharmacy and Biochemistry, Analytical Chemistry and Phisicochemistry Department, General and Inorganic Chemistry Division, Buenos Aires, Argentina; CONICET- University of Buenos Aires, Instituto de Bioquímica y Medicina Molecular (IBIMOL), Buenos Aires, Argenti
[Ti] Title:Diesel exhaust particles (DEP) induce an early redox imbalance followed by an IL-6 mediated inflammatory response on human conjunctival epithelial cells.
[So] Source:Exp Eye Res;, 2018 Mar 07.
[Is] ISSN:1096-0007
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:The aim of this study was to evaluate the time course of oxidative stress markers and inflammatory mediators in human conjunctival epithelial cells (IOBA-NHC) exposed to diesel exhaust particles (DEP) for 1, 3, and 24 h. Reactive oxygen species (ROS) production, lipid and protein oxidation, Nrf2 pathway activation, enzymatic antioxidants, glutathione (GSH) levels and synthesis, as well as cytokine release and cell proliferation were analyzed. Cells exposed to DEP showed an increase in ROS at all time points. The induction of NADPH oxidase-4 appeared later than mitochondrial superoxide anion production, when the cell also underwent a proinflammatory response mediated by IL-6. DEP exposure triggered the activation of Nrf2 in IOBA-NHC, as a strategy for increasing cellular antioxidant capacity. Antioxidant enzyme activities were significantly increased at early stages except for glutathione reductase (GR) that showed a significant decrease after a 3-h-incubation. GSH levels were found increased after 1 and 3 h of incubation with DEP, despite the increase in its consumption by the antioxidant enzymes as it works as a cofactor. GSH recycling and the de novo synthesis were responsible for the maintenance of its content at these time points, respectively. After 24 h, the decrease in GR and glutamate cysteine ligase as wells as the enhanced activity of glutathione peroxidase and glutathione S-transferase produced a depletion in the GSH pool. Lipid-peroxidation was found increased in cells exposed to DEP after 1-h-incubation, whereas protein oxidation was found increased in cells exposed to DEP after a 3-h-incubation that persisted after a longer exposure. Furthermore, DEP lead IOBA-NHC cells to hyperplasia after 1 and 3 h of incubation, but a decrease in cell proliferation was found after longer exposure. ROS production seems to be an earlier event triggered by DEP on IOBA-NHC, comparing to the proinflammatory response mediated by IL-6. Despite the fact that under short periods of exposure to DEP lipids and then proteins are targets of oxidative damage, the viability of the cells is not affected at early stages, since cell hyperplasia was detected as compensatory mechanism. Although after 24 h Nrf2 pathway is still enhanced, the epithelial cell capacity to maintain redox balance is exceeded. The antioxidant enzymes activation and the depleted GSH pool are not capable of counteracting the increased ROS production, leading to oxidative damage.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  9 / 458715 MEDLINE  
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[PMID]: 29514461
[Au] Autor:Moore IMK; Koerner KM; Gundy PM; Montgomery DW; Insel KC; Harris LL; Taylor OA; Hockenberry MJ
[Ad] Address:1 College of Nursing, The University of Arizona, Tucson, AZ, USA.
[Ti] Title:Changes in Oxidant Defense, Apoptosis, and Cognitive Abilities During Treatment for Childhood Leukemia.
[So] Source:Biol Res Nurs;:1099800418763124, 2018 Jan 01.
[Is] ISSN:1552-4175
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Aggressive central nervous system (CNS)-directed treatment for acute lymphoblastic leukemia (ALL), the most prevalent cancer among children and adolescents, prevents metastasis of leukemia cells into the brain. Up to 60% of survivors experience cognitive problems, but knowledge about risk factors for and mechanisms of neurologic injury is lacking. Objectives of the present study were to (1) quantify changes in oxidant defense and apoptosis over the course of ALL therapy and (2) elucidate risk factors for long-term cognitive problems. The sample included 71 children with ALL. Cerebrospinal fluid (CSF) samples were collected at diagnosis and during intrathecal chemotherapy administration. Oxidant defense was measured by reduced glutathione (GSH), oxidized glutathione (GSSG), and the ratio of GSH:GSSG. Apoptosis was measured by activity of several cysteine-dependent aspartate-specific protease (abbreviated as caspase) enzymes that initiate (caspases 8 and 9) or execute (caspases 3/7) apoptosis. Cognitive abilities were assessed by standardized measures of short-term memory, visual-motor integration, and attention 3 years after ALL diagnosis. GSH and GSSG concentration increased significantly during ALL therapy, and a low GSH:GSSG ratio was indicative of an oxidized extracellular environment. Caspase enzyme activity increased significantly, and caspases 3/7 activity was significantly and negatively associated with performance on measures of cognitive abilities. Younger age at time of ALL diagnosis was associated with some measures of attention. Efflux of glutathione into CSF maintains oxidant defense by scavenging free radicals and other reactive oxygen species and is an early event in apoptosis. These mechanisms may be involved in neurologic injury associated with CNS-directed treatment and subsequent cognitive problems.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:Publisher
[do] DOI:10.1177/1099800418763124

  10 / 458715 MEDLINE  
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[PMID]: 29511679
[Au] Autor:Xu F; Liu X; Wang C; Dai C
[Ad] Address:Department of Hepatobiliary and Spleen Surgery, Shengjing Hospital Affiliated to China Medical University, Shenyang, Liaoning 110004, China.
[Ti] Title:Prostaglandin E1 Preconditioning Attenuates Liver Ischemia Reperfusion Injury in a Rat Model of Extrahepatic Cholestasis.
[So] Source:Biomed Res Int;2018:3812424, 2018.
[Is] ISSN:2314-6141
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The aim of this study is to explore the hepatoprotective effect of intraportal prostaglandin E1 (PGE1) on liver ischemia reperfusion (IR) injury using an extrahepatic cholestatic model, observing oxidative stress markers, proinflammatory factors, apoptotic marker proteins, and an adhesion molecule. The extrahepatic cholestatic model was induced by common bile duct ligation. After seven days, rats were subjected to ischemia by Pringle maneuver for 15 min, followed by 1, 6, or 24 h of reperfusion. Prostaglandin E1 (PGE group) or normal saline (NS group) was continuously infused from 15 min before liver ischemia to 1 h after reperfusion. After reperfusion, histopathological evaluation of the liver was performed, as were measurements of bilirubin, biochemical enzymes, oxidative stress markers (GSH and MDA), proinflammatory factors (MPO, TNF- , and IL-1 ), apoptotic marker proteins (Bcl-2 and Bax), and the adhesion molecule (ICAM-1). PGE1 pretreatment attenuated IR injury in extrahepatic cholestatic liver probably by suppressing MDA, MPO, TNF- , IL-1 , ICAM-1, and Bax levels and improving GSH and Bcl-2 levels. In conclusion, PGE1 protects extrahepatic cholestatic liver from IR injury by improving hepatic microcirculation and reducing oxidative stress damage, intrahepatic neutrophil infiltration, and hepatocyte apoptosis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Process
[do] DOI:10.1155/2018/3812424


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