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Redox Biology

Aslihan Ugun-Klusek, Theodosis S Theodosi, Julia C Fitzgerald, Florence Burté, Christoph Ufer, David J Boocock, Patrick Yu-Wai-Man, Lynn Bedford, E Ellen Billett
Monoamine oxidases (MAOs) are located on the outer mitochondrial membrane and are drug targets for the treatment of neurological disorders. MAOs control the levels of neurotransmitters in the brain via oxidative deamination and contribute to reactive oxygen species (ROS) generation through their catalytic by-product H2 O2 . Increased ROS levels may modulate mitochondrial function and mitochondrial dysfunction is implicated in a vast array of disorders. However, the downstream effects of MAO-A mediated ROS production in a neuronal model has not been previously investigated...
October 9, 2018: Redox Biology
Nan Xu, Qin Wang, Shan Jiang, Qijing Wang, Weipeng Hu, Suhan Zhou, Liang Zhao, Lanyu Xie, Jianghua Chen, Anton Wellstein, En Yin Lai
Fenofibrate, a peroxisome proliferator-activated receptors α (PPARα) agonist, reduces vascular complications of diabetic patients but its protective mechanisms are not fully understood. Here we tested the hypothesis that fenofibrate improves vascular endothelial dysfunction by balancing endothelium-dependent relaxation and contractility of the aorta in diabetes mellitus (DM). In streptozotocin-induced diabetic mice, eight weeks of fenofibrate treatment (100 mg/Kg/d) improved endothelium dependent relaxation in the macro- and microvessels, increased nitric oxide (NO) levels, reduced renal damage markers and effects of the vasoconstrictor prostaglandin...
October 1, 2018: Redox Biology
Naveen K Mekala, Jacob Kurdys, Mikayla M Depuydt, Edwin J Vazquez, Mariana G Rosca
Dysfunction in mitochondrial oxidative phosphorylation (OXPHOS) underlies a wide spectrum of human ailments known as mitochondrial diseases. Deficiencies in complex I of the electron transport chain (ETC) contribute to 30-40% of all cases of mitochondrial diseases, and leads to eye disease including optic nerve atrophy and retinal degeneration. The mechanisms responsible for organ damage in mitochondrial defects may include energy deficit, oxidative stress, and an increase in the NADH/NAD+ redox ratio due to decreased NAD+ regeneration...
September 29, 2018: Redox Biology
Jun Mo, Budbazar Enkhjargal, Zachary D Travis, Keren Zhou, Pei Wu, Guangyu Zhang, Qiquan Zhu, Tongyu Zhang, Jianhua Peng, Weilin Xu, Umut Ocak, Yili Chen, Jiping Tang, Jianmin Zhang, John H Zhang
Oxidative stress and neuronal apoptosis have been demonstrated to be key features in early brain injury (EBI) after subarachnoid hemorrhage (SAH). Previous studies have indicated that Mas receptor activation initiates an anti-oxidative and anti-apoptotic role in the brain. However, whether Mas activation can attenuate oxidative stress and neuronal apoptosis after SAH remains unknown. To investigate the beneficial effect of Mas on oxidative stress injury and neuronal apoptosis induced by SAH, a total of 196 rats were subjected to an endovascular perforation model of SAH...
September 28, 2018: Redox Biology
Kranti A Mapuskar, Hsiang Wen, Danniele G Holanda, Prerna Rastogi, Emily Steinbach, Rachel Han, Mitchell C Coleman, Massimo Attanasio, Dennis P Riley, Douglas R Spitz, Bryan G Allen, Diana Zepeda-Orozco
Severe and recurrent cisplatin-induced acute kidney injury (AKI) as part of standard cancer therapy is a known risk factor for development of chronic kidney disease (CKD). The specific role of superoxide (O2 •- )-mediated disruption of mitochondrial oxidative metabolism in CKD after cisplatin treatment is unexplored. Cisplatin is typically administered in weekly or tri-weekly cycles as part of standard cancer therapy. To investigate the role of O2 •- in predisposing patients to future renal injury and in CKD, mice were treated with cisplatin and a mitochondrial-specific, superoxide dismutase (SOD) mimetic, GC4419...
September 27, 2018: Redox Biology
Rizwan Qaisar, Shylesh Bhaskaran, Rojina Ranjit, Kavithalakshmi Sataranatarajan, Pavithra Premkumar, Kendra Huseman, Holly Van Remmen
Molecular targets to reduce muscle weakness and atrophy due to oxidative stress have been elusive. Here we show that activation of Sarcoplasmic Reticulum (SR) Ca2+ ATPase (SERCA) with CDN1163, a novel small molecule allosteric SERCA activator, ameliorates the muscle impairment in the CuZnSOD deficient (Sod1-/- ) mouse model of oxidative stress. Sod1-/- mice are characterized by reduced SERCA activity, muscle weakness and atrophy, increased oxidative stress and mitochondrial dysfunction. Seven weeks of CDN1163 treatment completely restored SERCA activity and reversed the 23% reduction in gastrocnemius mass and 22% reduction in specific force in untreated Sod1-/- versus wild type mice...
September 27, 2018: Redox Biology
Niklas Jänsch, Christian Meyners, Marius Muth, Aleksandra Kopranovic, Olaf Witt, Ina Oehme, Franz-Josef Meyer-Almes
Enzymes from the histone deacetylase (HDAC) family are highly regulated by different mechanisms. However, only very limited knowledge exists about the regulation of HDAC8, an established target in multiple types of cancer. A previous dedicated study of HDAC class I enzymes identified no redox-sensitive cysteinyl thiol in HDAC8. This is in contrast to the observation that HDAC8 preparations show different enzyme activities depending on the addition of reducing agents. In the light of the importance of HDAC8 in tumorigenesis a possible regulation by redox signaling was investigated using biochemical and biophysical methods combined with site directed mutagenesis...
September 27, 2018: Redox Biology
Yang Yang, Ling Li, Qiyun Hang, Yuan Fang, Xiaoliang Dong, Peng Cao, Zhimin Yin, Lan Luo
Sepsis is a life-threatening organ dysfunction caused by dysregulated host response to infection and characterized by redox imbalance and severe oxidative stress. Glutathione (GSH) serves several vital functions, including scavenging free radicals and maintaining intracellular redox balance. Extracellular GSH is unable to be taken into the majority of human cells, and the GSH prodrug N-acetyl-l-cysteine (NAC) does not exhibit promising clinical effects. γ-glutamylcysteine (γ-GC), an intermediate dipeptide of the GSH-synthesis pathway and harboring anti-inflammatory properties, represents a relatively unexplored option for sepsis treatment...
September 26, 2018: Redox Biology
Klaus Mayer, Olaf Mundigl, Hubert Kettenberger, Fabian Birzele, Sebastian Stahl, Ira Pastan, Ulrich Brinkmann
The diphthamide modification of translation elongation factor 2 is highly conserved in eukaryotes and archaebacteria. Nevertheless, cells lacking diphthamide can carry out protein synthesis and are viable. We have analyzed the phenotypes of diphthamide deficient cells and found that diphthamide deficiency reduces selenocysteine incorporation into selenoproteins. Additional phenotypes resulting from diphthamide deficiency include altered tRNA-synthetase and selenoprotein transcript levels, hypersensitivity to oxidative stress and increased selenite tolerance...
September 26, 2018: Redox Biology
Xun Wu, Lihui Zhang, Yütong Miao, Juan Yang, Xian Wang, Chih-Chen Wang, Juan Feng, Lei Wang
Endothelial dysfunction induced by hyperhomocysteinemia (HHcy) plays a critical role in vascular pathology. However, little is known about the role of endoplasmic reticulum (ER) redox homeostasis in HHcy-induced endothelial dysfunction. Here, we show that Hcy induces ER oxidoreductin-1α (Ero1α) expression with ER stress and inflammation in human umbilical vein endothelial cells and in the arteries of HHcy mice. Hcy upregulates Ero1α expression by promoting binding of hypoxia-inducible factor 1α to the ERO1A promoter...
September 26, 2018: Redox Biology
Ruth Liliám Quispe, Michael Lorenz Jaramillo, Leticia Selinger Galant, Daiane Engel, Alcir Luiz Dafre, João Batista Teixeira da Rocha, Rafael Radi, Marcelo Farina, Andreza Fabro de Bem
Oxidative stress and mitochondrial dysfunction are critical events in neurodegenerative diseases; therefore, molecules that increase cellular antioxidant defenses represent a future pharmacologic strategy to counteract such conditions. The aim of this study was to investigate the potential protective effect of (PhSe)2 on mouse hippocampal cell line (HT22) exposed to tert-BuOOH (in vitro model of oxidative stress), as well as to elucidate potential mechanisms underlying this protection. Our results showed that tert-BuOOH caused time- and concentration-dependent cytotoxicity, which was preceded by increased oxidants production and mitochondrial dysfunction...
September 25, 2018: Redox Biology
Min Jung Kong, Sang Hong Bak, Ki-Hwan Han, Jee In Kim, Jeen-Woo Park, Kwon Moo Park
The primary cilium, which protrudes from the cell surface, is associated with the pathogenesis of various diseases, including acute kidney injury (AKI). Primary cilium length dynamically changes during the progression of diseases. However, its relevance in disease and the underlying mechanism are largely unknown. In this study, we investigated the role of primary cilia in AKI induced by cisplatin, an effective anticancer drug, and the underlying mechanisms. In addition, we evaluated the usefulness of length alteration and deciliation of primary cilia into the urine for the diagnosis of AKI...
September 25, 2018: Redox Biology
M E Solovieva, Yu V Shatalin, V V Solovyev, A V Sazonov, V P Kutyshenko, V S Akatov
It is known that some metals (Cu, Zn, Cd, Au) markedly increase the toxic effect of thiocarbamates. It was shown in the present study that hydroxycobalamin (a form of vitamin B12 , HOCbl), which incorporates cobalt, significantly enhances the cytotoxicity of diethyldithiocarbamate (DDC), decreasing its IC50 value in tumor cells three to five times. The addition of HOCbl to aqueous DDC solutions accelerated the reduction of oxygen. No hydrogen peroxide accumulation was observed in DDC + HOCbl solutions; however, catalase slowed down the oxygen reduction rate...
September 25, 2018: Redox Biology
Ming-Horng Tsai, Chiang-Wen Lee, Lee-Fen Hsu, Shu-Yu Li, Yao-Chang Chiang, Ming-Hsueh Lee, Chun-Han Chen, Hwey-Fang Liang, Jia-Mei How, Pey-Jium Chang, Ching-Mei Wu, I-Ta Lee
No abstract text is available yet for this article.
September 24, 2018: Redox Biology
Andrea Gille, Abdullah Turkistani, Dimitrios Tsitsipatis, Xiaoqing Hou, Sarah Tauber, Ingrit Hamann, Nadine Urban, Katrin Erler, Holger Steinbrenner, Lars-Oliver Klotz
Diethyl maleate (DEM), a thiol-reactive α,β-unsaturated carbonyl compound, depletes glutathione (GSH) in exposed cells and was previously shown by us to elicit a stress response in Caenorhabditis elegans that, at lower concentrations, results in enhanced stress resistance and longer lifespan. This hormetic response was mediated through both the Nrf2 ortholog, SKN-1, and the forkhead box O (FOXO) family transcription factor DAF-16. As FOXO signaling is evolutionarily conserved, we analyzed here the effects of DEM exposure on FOXO in cultured human cells (HepG2, HEK293)...
September 14, 2018: Redox Biology
Szabolcs Felszeghy, Johanna Viiri, Jussi J Paterno, Juha M T Hyttinen, Ali Koskela, Mei Chen, Henri Leinonen, Heikki Tanila, Niko Kivinen, Arto Koistinen, Elisa Toropainen, Marialaura Amadio, Adrian Smedowski, Mika Reinisalo, Mateusz Winiarczyk, Jerzy Mackiewicz, Maija Mutikainen, Anna-Kaisa Ruotsalainen, Mikko Kettunen, Kimmo Jokivarsi, Debasish Sinha, Kati Kinnunen, Goran Petrovski, Janusz Blasiak, Geir Bjørkøy, Ari Koskelainen, Heli Skottman, Arto Urtti, Antero Salminen, Ram Kannan, Deborah A Ferrington, Heping Xu, Anna-Liisa Levonen, Pasi Tavi, Anu Kauppinen, Kai Kaarniranta
Age-related macular degeneration (AMD) is a multi-factorial disease that is the leading cause of irreversible and severe vision loss in the developed countries. It has been suggested that the pathogenesis of dry AMD involves impaired protein degradation in retinal pigment epithelial cells (RPE). RPE cells are constantly exposed to oxidative stress that may lead to the accumulation of damaged cellular proteins, DNA and lipids and evoke tissue deterioration during the aging process. The ubiquitin-proteasome pathway and the lysosomal/autophagosomal pathway are the two major proteolytic systems in eukaryotic cells...
September 14, 2018: Redox Biology
Agnes Keszler, Brian Lindemer, Neil Hogg, Nicole L Lohr
There is significant therapeutic advantage of nitric oxide synthase (NOS) independent nitric oxide (NO) production in maladies where endothelium, and thereby NOS, is dysfunctional. Electromagnetic radiation in the red and near infrared region has been shown to stimulate NOS-independent but NO-dependent vasodilation, and thereby has significant therapeutic potential. We have recently shown that red light induces acute vasodilatation in the pre-constricted murine facial artery via the release of an endothelium derived substance...
September 10, 2018: Redox Biology
Marcel Imber, Agnieszka J Pietrzyk-Brzezinska, Haike Antelmann
Low molecular weight (LMW) thiols play an important role as thiol-cofactors for many enzymes and are crucial to maintain the reduced state of the cytoplasm. Most Gram-negative bacteria utilize glutathione (GSH) as major LMW thiol. However, in Gram-positive Actinomycetes and Firmicutes alternative LMW thiols, such as mycothiol (MSH) and bacillithiol (BSH) play related roles as GSH surrogates, respectively. Under conditions of hypochlorite stress, MSH and BSH are known to form mixed disulfides with protein thiols, termed as S-mycothiolation or S-bacillithiolation that function in thiol-protection and redox regulation...
August 24, 2018: Redox Biology
Ying-Qian Han, Sheng-Li Ming, Hong-Tao Wu, Lei Zeng, Gen Ba, Jian Li, Wei-Fei Lu, Jie Han, Qia-Jun Du, Miao-Miao Sun, Guo-Yu Yang, Jiang Wang, Bei-Bei Chu
Myostatin (Mstn) is postulated to be a key determinant of muscle loss and cachexia in cancer. However, no experimental evidence supports a role for Mstn in cancer, particularly in regulating the survival and growth of cancer cells. In this study, we showed that the expression of Mstn was significantly increased in different tumor tissues and human cancer cells. Mstn knockdown inhibited the proliferation of cancer cells. A knockout (KO) of Mstn created by clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein (Cas) 9 (CRISPR/Cas9) induced mitochondria-dependent apoptosis in HeLa cells...
October 2018: Redox Biology
Sarah E Lacher, Daniel C Levings, Samuel Freeman, Matthew Slattery
Reactive oxygen species (ROS), which are a byproduct of oxidative metabolism, serve as signaling molecules in a number of physiological settings. However, if their levels are not tightly maintained, excess ROS lead to potentially cytotoxic oxidative stress. Accordingly, several transcriptional regulatory networks have evolved to include components that are highly ROS-responsive. Depending on the context, these regulatory networks can leverage ROS to respond to nutrient conditions, metabolism, or other physiological signals, or to respond to oxidative stress...
October 2018: Redox Biology
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