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Redox Biology

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https://www.readbyqxmd.com/read/28646795/offsetting-the-impact-of-smoking-and-e-cigarette-vaping-on-the-cerebrovascular-system-and-stroke-injury-is-metformin-a-viable-countermeasure
#1
Mohammad A Kaisar, Heidi Villalba, Shikha Prasad, Taylor Liles, Ali Ehsan Sifat, Ravi K Sajja, Thomas J Abbruscato, Luca Cucullo
Recently published in vitro and in vivo findings strongly suggest that BBB impairment and increased risk for stroke by tobacco smoke (TS) closely resemble that of type-2 diabetes (2DM) and develop largely in response to common key modulators such oxidative stress (OS), inflammation and alterations of the endogenous antioxidative response system (ARE) regulated by the nuclear factor erythroid 2-related factor (Nrf2). Preclinical studies have also shown that nicotine (the principal e-liquid's ingredient used in e-cigarettes) can also cause OS, exacerbation of cerebral ischemia and secondary brain injury...
June 17, 2017: Redox Biology
https://www.readbyqxmd.com/read/28646794/dexibuprofen-prevents-neurodegeneration-and-cognitive-decline-in-appswe-ps1de9-through-multiple-signaling-pathways
#2
Miren Ettcheto, Elena Sánchez-López, Laura Pons, Oriol Busquets, Jordi Olloquequi, Carlos Beas-Zarate, Merce Pallas, Maria Luisa García, Carme Auladell, Jaume Folch, Antoni Camins
The aim of the present study is to elucidate the neuronal pathways associated to NSAIDs causing a reduction of the risk and progression of Alzheimer's disease. The research was developed administering the active enantiomer of ibuprofen, dexibuprofen (DXI), in order to reduce associated gastric toxicity. DXI was administered from three to six-month-old female APPswe/PS1dE9 mice as a model of familial Alzheimer's disease. DXI treatment reduced the activation of glial cells and the cytokine release involved in the neurodegenerative process, especially TNFα...
June 15, 2017: Redox Biology
https://www.readbyqxmd.com/read/28633109/endothelial-nlrp3-inflammasome-activation-and-arterial-neointima-formation-associated-with-acid-sphingomyelinase-during-hypercholesterolemia
#3
Saisudha Koka, Min Xia, Yang Chen, Owais M Bhat, Xinxu Yuan, Krishna M Boini, Pin-Lan Li
The NLRP3 inflammasome has been reported to be activated by atherogenic factors, whereby endothelial injury and consequent atherosclerotic lesions are triggered in the arterial wall. However, the mechanisms activating and regulating NLRP3 inflammasomes remain poorly understood. The present study tested whether acid sphingomyelinase (ASM) and ceramide associated membrane raft (MR) signaling platforms contribute to the activation of NLRP3 inflammasomes and atherosclerotic lesions during hypercholesterolemia. We found that 7-ketocholesterol (7-Keto) or cholesterol crystal (ChC) markedly increased the formation and activation of NLRP3 inflammasomes in mouse carotid arterial endothelial cells (CAECs), as shown by increased colocalization of NLRP3 with ASC or caspase-1, enhanced caspase-1 activity and elevated IL-1β levels, which were markedly attenuated by mouse Asm siRNA, ASM inhibitor- amitriptyline, and deletion of mouse Asm gene...
June 15, 2017: Redox Biology
https://www.readbyqxmd.com/read/28623824/dietary-nitrate-attenuates-renal-ischemia-reperfusion-injuries-by-modulation-of-immune-responses-and-reduction-of-oxidative-stress
#4
Ting Yang, Xing-Mei Zhang, Laura Tarnawski, Maria Peleli, Zhengbing Zhuge, Niccolo Terrando, Robert A Harris, Peder S Olofsson, Erik Larsson, A Erik G Persson, Jon O Lundberg, Eddie Weitzberg, Mattias Carlstrom
Ischemia-reperfusion (IR) injury involves complex pathological processes in which reduction of nitric oxide (NO) bioavailability is suggested as a key factor. Inorganic nitrate can form NO in vivo via NO synthase-independent pathways and may thus provide beneficial effects during IR. Herein we evaluated the effects of dietary nitrate supplementation in a renal IR model. Male mice (C57BL/6J) were fed nitrate-supplemented chow (1.0mmol/kg/day) or standard chow for two weeks prior to 30min ischemia and during the reperfusion period...
June 9, 2017: Redox Biology
https://www.readbyqxmd.com/read/28600985/nox2-contributes-to-hyperinsulinemia-induced-redox-imbalance-and-impaired-vascular-function
#5
Abeer M Mahmoud, Mohamed M Ali, Edwin R Miranda, Jacob T Mey, Brian K Blackburn, Jacob M Haus, Shane A Phillips
Insulin resistance promotes vascular endothelial dysfunction and subsequent development of cardiovascular disease. Previously we found that skeletal muscle arteriolar flow-induced dilation (FID) was reduced following a hyperinsulinemic clamp in healthy adults. Therefore, we hypothesized that hyperinsulinemia, a hallmark of insulin resistance, contributes to microvascular endothelial cell dysfunction via inducing oxidative stress that is mediated by NADPH oxidase (Nox) system. We examined the effect of insulin, at levels that are comparable with human hyperinsulinemia on 1) FID of isolated arterioles from human skeletal muscle tissue in the presence and absence of Nox inhibitors and 2) human adipose microvascular endothelial cell (HAMECs) expression of nitric oxide (NO), endothelial NO synthase (eNOS), and Nox-mediated oxidative stress...
June 3, 2017: Redox Biology
https://www.readbyqxmd.com/read/28601780/sirt1-inhibition-causes-oxidative-stress-and-inflammation-in-patients-with-coronary-artery-disease
#6
Shih-Hung Chan, Ching-Hsia Hung, Jhih-Yuan Shih, Pei-Ming Chu, Yung-Hsin Cheng, Huei-Chen Lin, Kun-Ling Tsai
Coronary artery disease (CAD) is the primary critical cardiovascular event. Endothelial cell and monocyte dysfunction with subsequent extravagant inflammation are the main causes of vessel damage in CAD. Thus, strategies that repress cell death and manage unsuitable pro-inflammatory responses in CAD are potential therapeutic strategies for improving the clinical prognosis of patients with CAD. SIRT1 (Sirtuin 1) plays an important role in regulating cellular physiological processes. SIRT1 is also thought to protect the cardiovascular system by means of its antioxidant, anti-inflammation and anti-apoptosis activities...
June 2, 2017: Redox Biology
https://www.readbyqxmd.com/read/28600984/impaired-cross-talk-between-the-thioredoxin-and-glutathione-systems-is-related-to-ask-1-mediated-apoptosis-in-neuronal-cells-exposed-to-mercury
#7
Vasco Branco, Lucia Coppo, Susana Solá, Jun Lu, Cecília M P Rodrigues, Arne Holmgren, Cristina Carvalho
Mercury (Hg) compounds target both cysteine (Cys) and selenocysteine (Sec) residues in peptides and proteins. Thus, the components of the two major cellular antioxidant systems - glutathione (GSH) and thioredoxin (Trx) systems - are likely targets for mercurials. Hg exposure results in GSH depletion and Trx and thioredoxin reductase (TrxR) are prime targets for mercury. These systems have a wide-range of common functions and interaction between their components has been reported. However, toxic effects over both systems are normally treated as isolated events...
June 1, 2017: Redox Biology
https://www.readbyqxmd.com/read/28600982/altered-bioenergetics-and-enhanced-resistance-to-oxidative-stress-in-human-retinal-pigment-epithelial-cells-from-donors-with-age-related-macular-degeneration
#8
Deborah A Ferrington, Mara C Ebeling, Rebecca J Kapphahn, Marcia R Terluk, Cody R Fisher, Jorge R Polanco, Heidi Roehrich, Michaela M Leary, Zhaohui Geng, James R Dutton, Sandra R Montezuma
Age-related macular degeneration (AMD) is the leading cause of blindness among older adults. It has been suggested that mitochondrial defects in the retinal pigment epithelium (RPE) underlies AMD pathology. To test this idea, we developed primary cultures of RPE to ask whether RPE from donors with AMD differ in their metabolic profile compared with healthy age-matched donors. Analysis of gene expression, protein content, and RPE function showed that these cultured cells replicated many of the cardinal features of RPE in vivo...
June 1, 2017: Redox Biology
https://www.readbyqxmd.com/read/28582730/rita-plus-3-ma-overcomes-chemoresistance-of-head-and-neck-cancer-cells-via-dual-inhibition-of-autophagy-and-antioxidant-systems
#9
Daiha Shin, Eun Hye Kim, Jaewang Lee, Jong-Lyel Roh
Reactivation of p53 and induction of tumor cell apoptosis (RITA) is a small molecule that blocks p53-MDM2 interaction, thereby reactivating p53 in tumors. RITA can induce exclusive apoptosis in cancer cells independently of the p53 pathway; however, the resistance of cancer cells remains a major drawback. Here, we found a novel resistance mechanism of RITA treatment and an effective combined treatment to overcome RITA resistance in head and neck cancer (HNC) cells. The effects of RITA and 3-methyladenine (3-MA) were tested in different HNC cell lines, including cisplatin-resistant and acquired RITA-resistant HNC cells...
June 1, 2017: Redox Biology
https://www.readbyqxmd.com/read/28624704/maintenance-of-redox-homeostasis-by-hypoxia-inducible-factors
#10
REVIEW
Debangshu Samanta, Gregg L Semenza
Oxidative phosphorylation enables cells to generate the large amounts of ATP required for development and maintenance of multicellular organisms. However, under conditions of reduced O2 availability, electron transport becomes less efficient, leading to increased generation of superoxide anions. Hypoxia-inducible factors switch cells from oxidative to glycolytic metabolism, to reduce mitochondrial superoxide generation, and increase the synthesis of NADPH and glutathione, in order to maintain redox homeostasis under hypoxic conditions...
May 31, 2017: Redox Biology
https://www.readbyqxmd.com/read/28601781/cysteine-residues-244-and-458-459-within-the-catalytic-subunit-of-na-k-atpase-control-the-enzyme-s-hydrolytic-and-signaling-function-under-hypoxic-conditions
#11
Irina Yu Petrushanko, Vladimir A Mitkevich, Valentina A Lakunina, Anastasia A Anashkina, Pavel V Spirin, Peter M Rubtsov, Vladimir S Prassolov, Nikolay B Bogdanov, Pascal Hänggi, William Fuller, Alexander A Makarov, Anna Bogdanova
Our previous findings suggested that reversible thiol modifications of cysteine residues within the actuator (AD) and nucleotide binding domain (NBD) of the Na,K-ATPase may represent a powerful regulatory mechanism conveying redox- and oxygen-sensitivity of this multifunctional enzyme. S-glutathionylation of Cys244 in the AD and Cys 454-458-459 in the NBD inhibited the enzyme and protected cysteines' thiol groups from irreversible oxidation under hypoxic conditions. In this study mutagenesis approach was used to assess the role these cysteines play in regulation of the Na,K-ATPase hydrolytic and signaling functions...
May 31, 2017: Redox Biology
https://www.readbyqxmd.com/read/28600981/pharmacologic-concentrations-of-linezolid-modify-oxidative-phosphorylation-function-and-adipocyte-secretome
#12
Laura Llobet, M Pilar Bayona-Bafaluy, David Pacheu-Grau, Elena Torres-Pérez, José M Arbones-Mainar, M Ángeles Navarro, Covadonga Gómez-Díaz, Julio Montoya, Ester López-Gallardo, Eduardo Ruiz-Pesini
The oxidative phosphorylation system is important for adipocyte differentiation. Therefore, xenobiotics inhibitors of the oxidative phosphorylation system could affect adipocyte differentiation and adipokine secretion. As adipokines impact the overall health status, these xenobiotics may have wide effects on human health. Some of these xenobiotics are widely used therapeutic drugs, such as ribosomal antibiotics. Because of its similarity to the bacterial one, mitochondrial translation system is an off-target for these compounds...
May 31, 2017: Redox Biology
https://www.readbyqxmd.com/read/28595160/redox-signaling-during-hypoxia-in-mammalian-cells
#13
REVIEW
Kimberly A Smith, Gregory B Waypa, Paul T Schumacker
Hypoxia triggers a wide range of protective responses in mammalian cells, which are mediated through transcriptional and post-translational mechanisms. Redox signaling in cells by reactive oxygen species (ROS) such as hydrogen peroxide (H2O2) occurs through the reversible oxidation of cysteine thiol groups, resulting in structural modifications that can change protein function profoundly. Mitochondria are an important source of ROS generation, and studies reveal that superoxide generation by the electron transport chain increases during hypoxia...
May 31, 2017: Redox Biology
https://www.readbyqxmd.com/read/28582729/the-role-of-nrf1-and-nrf2-in-the-regulation-of-glutathione-and-redox-dynamics-in-the-developing-zebrafish-embryo
#14
Karilyn E Sant, Jason M Hansen, Larissa M Williams, Nancy L Tran, Jared V Goldstone, John J Stegeman, Mark E Hahn, Alicia Timme-Laragy
Redox signaling is important for embryogenesis, guiding pathways that govern processes crucial for embryo patterning, including cell polarization, proliferation, and apoptosis. Exposure to pro-oxidants during this period can be deleterious, resulting in altered physiology, teratogenesis, later-life diseases, or lethality. We previously reported that the glutathione antioxidant defense system becomes increasingly robust, including a doubling of total glutathione and dynamic shifts in the glutathione redox potential at specific stages during embryonic development in the zebrafish, Danio rerio...
May 30, 2017: Redox Biology
https://www.readbyqxmd.com/read/28600983/hpw-rx40-prevents-human-platelet-activation-by-attenuating-cell-surface-protein-disulfide-isomerases
#15
Po-Hsiung Kung, Pei-Wen Hsieh, Ying-Ting Lin, Jia-Hau Lee, I-Hua Chen, Chin-Chung Wu
Protein disulfide isomerase (PDI) present at platelet surfaces has been considered to play an important role in the conformational change and activation of the integrin glycoprotein IIb/IIIa (GPIIb/IIIa) and thus enhances platelet aggregation. Growing evidences indicated that platelet surface PDI may serve as a potential target for developing of a new class of antithrombotic agents. In the present study, we investigated the effects of HPW-RX40, a chemical derivative of β-nitrostyrene, on platelet activation and PDI activity...
May 29, 2017: Redox Biology
https://www.readbyqxmd.com/read/28582728/mitochondrial-aldehyde-dehydrogenase-2-deficiency-compromises-therapeutic-effect-of-aldh-bright-cell-on-peripheral-ischemia
#16
Xiaolei Sun, Hong Zhu, Zhen Dong, Xiangwei Liu, Xin Ma, Shasha Han, Fei Lu, Peng Wang, Sanli Qian, Cong Wang, Cheng Shen, Xiaona Zhao, Yunzeng Zou, Junbo Ge, Aijun Sun
The autologous ALDH bright (ALDH(br)) cell therapy for ischemic injury is clinically safe and effective, while the underlying mechanism remains elusive. Here, we demonstrated that the glycolysis dominant metabolism of ALDH(br) cells is permissive to restore blood flow in an ischemic hind limb model compared with bone marrow mononuclear cells (BMNCs). PCR array analysis showed overtly elevated Aldh2 expression of ALDH(br) cells following hypoxic challenge. Notably, ALDH(br) cells therapy induced blood flow recovery in this model was reduced in case of ALDH2 deficiency...
May 29, 2017: Redox Biology
https://www.readbyqxmd.com/read/28578276/decoding-nadph-oxidase-4-expression-in-human-tumors
#17
Jennifer L Meitzler, Hala R Makhlouf, Smitha Antony, Yongzhong Wu, Donna Butcher, Guojian Jiang, Agnes Juhasz, Jiamo Lu, Iris Dahan, Pidder Jansen-Dürr, Haymo Pircher, Ajay M Shah, Krishnendu Roy, James H Doroshow
NADPH oxidase 4 (NOX4) is a redox active, membrane-associated protein that contributes to genomic instability, redox signaling, and radiation sensitivity in human cancers based on its capacity to generate H2O2 constitutively. Most studies of NOX4 in malignancy have focused on the evaluation of a small number of tumor cell lines and not on human tumor specimens themselves; furthermore, these studies have often employed immunological tools that have not been well characterized. To determine the prevalence of NOX4 expression across a broad range of solid tumors, we developed a novel monoclonal antibody that recognizes a specific extracellular region of the human NOX4 protein, and that does not cross-react with any of the other six members of the NOX gene family...
May 26, 2017: Redox Biology
https://www.readbyqxmd.com/read/28578274/synthesis-and-characterization-of-a-novel-organic-nitrate-ndhp-role-of-xanthine-oxidoreductase-mediated-nitric-oxide-formation
#18
Zhengbing Zhuge, Luciano L Paulo, Arghavan Jahandideh, Maria C R Brandão, Petrônio F Athayde-Filho, Jon O Lundberg, Valdir A Braga, Mattias Carlström, Marcelo F Montenegro
In this report, we describe the synthesis and characterization of 1,3-bis(hexyloxy)propan-2-yl nitrate (NDHP), a novel organic mono nitrate. Using purified xanthine oxidoreductase (XOR), chemiluminescence and electron paramagnetic resonance (EPR) spectroscopy, we found that XOR catalyzes nitric oxide (NO) generation from NDHP under anaerobic conditions, and that thiols are not involved or required in this process. Further mechanistic studies revealed that NDHP could be reduced to NO at both the FAD and the molybdenum sites of XOR, but that the FAD site required an unoccupied molybdenum site...
May 26, 2017: Redox Biology
https://www.readbyqxmd.com/read/28575743/igf-ii-promotes-neuroprotection-and-neuroplasticity-recovery-in-a-long-lasting-model-of-oxidative-damage-induced-by-glucocorticoids
#19
E Martín-Montañez, C Millon, F Boraldi, F Garcia-Guirado, C Pedraza, E Lara, L J Santin, J Pavia, M Garcia-Fernandez
Insulin-like growth factor-II (IGF-II) is a naturally occurring hormone that exerts neurotrophic and neuroprotective properties in a wide range of neurodegenerative diseases and ageing. Accumulating evidence suggests that the effects of IGF-II in the brain may be explained by its binding to the specific transmembrane receptor, IGFII/M6P receptor (IGF-IIR). However, relatively little is known regarding the role of IGF-II through IGF-IIR in neuroprotection. Here, using adult cortical neuronal cultures, we investigated whether IGF-II exhibits long-term antioxidant effects and neuroprotection at the synaptic level after oxidative damage induced by high and transient levels of corticosterone (CORT)...
May 26, 2017: Redox Biology
https://www.readbyqxmd.com/read/28578275/mitochondria-meditated-pathways-of-organ-failure-upon-inflammation
#20
REVIEW
Andrey V Kozlov, Jack R Lancaster, Andras T Meszaros, Adelheid Weidinger
Liver failure induced by systemic inflammatory response (SIRS) is often associated with mitochondrial dysfunction but the mechanism linking SIRS and mitochondria-mediated liver failure is still a matter of discussion. Current hypotheses suggest that causative events could be a drop in ATP synthesis, opening of mitochondrial permeability transition pore, specific changes in mitochondrial morphology, impaired Ca(2+) uptake, generation of mitochondrial reactive oxygen species (mtROS), turnover of mitochondria and imbalance in electron supply to the respiratory chain...
May 25, 2017: Redox Biology
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