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https://www.readbyqxmd.com/read/29864244/effect-of-a-mitochondrial-targeted-coenzyme-q-analog-on-pancreatic-%C3%AE-cell-function-and-energetics-in-high-fat-fed-obese-mice
#1
Yumi Imai, Brian D Fink, Joseph A Promes, Chaitanya A Kulkarni, Robert J Kerns, William I Sivitz
We recently reported that mitoquinone (mitoQ, 500 μmol/L) added to drinking water of C57BL/6J mice attenuated weight gain and reduced oxidative stress when administered to high-fat (HF) fed mice. Here, we examined the effects of mitoQ administered to HF fed mice on pancreatic islet morphology, dynamics of insulin secretion, and islet mitochondrial metabolism. C57BL/6J mice were fed HF for 130 days while we administered vehicle (cyclodextrin [CD]) or mitoQ added to the drinking water at up to 500 μmol/L...
June 2018: Pharmacology Research & Perspectives
https://www.readbyqxmd.com/read/29842922/mitoq-protects-dopaminergic-neurons-in-a-6-ohda-induced-pd-model-by-enhancing-mfn2-dependent-mitochondrial-fusion-via-activation-of-pgc-1%C3%AE
#2
Ye Xi, Dayun Feng, Kai Tao, Ronglin Wang, Yajun Shi, Huaizhou Qin, Michael P Murphy, Qian Yang, Gang Zhao
Parkinson's disease (PD) is characterized by the degeneration of dopaminergic neurons in the substantia nigra compacta (SNc). Although mitochondrial dysfunction is the critical factor in the pathogenesis of PD, the underlying molecular mechanisms are not well understood, and as a result, effective medical interventions are lacking. Mitochondrial fission and fusion play important roles in the maintenance of mitochondrial function and cell viability. Here, we investigated the effects of MitoQ, a mitochondria-targeted antioxidant, in 6-hydroxydopamine (6-OHDA)-induced in vitro and in vivo PD models...
May 26, 2018: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/29783748/neuronal-dysfunction-associated-with-cholesterol-deregulation
#3
Annalisa Marcuzzi, Claudia Loganes, Erica Valencic, Elisa Piscianz, Lorenzo Monasta, Sabrine Bilel, Roberta Bortul, Claudio Celeghini, Marina Zweyer, Alberto Tommasini
Cholesterol metabolism is crucial for cells and, in particular, its biosynthesis in the central nervous system occurs in situ, and its deregulation involves morphological changes that cause functional variations and trigger programmed cell death. The pathogenesis of rare diseases, such as Mevalonate Kinase Deficiency or Smith⁻Lemli⁻Opitz Syndrome, arises due to enzymatic defects in the cholesterol metabolic pathways, resulting in a shortage of downstream products. The most severe clinical manifestations of these diseases appear as neurological defects...
May 19, 2018: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/29778808/maternal-treatment-with-a-placental-targeted-antioxidant-mitoq-impacts-offspring-cardiovascular-function-in-a-rat-model-of-prenatal-hypoxia
#4
Mais M Aljunaidy, Jude S Morton, Raven Kirschenman, Tom Phillips, C Patrick Case, Christy-Lynn M Cooke, Sandra T Davidge
Intrauterine growth restriction, a common consequence of prenatal hypoxia, is a leading cause of fetal morbidity and mortality with a significant impact on population health. Hypoxia may increase placental oxidative stress and lead to an abnormal release of placental-derived factors, which are emerging as potential contributors to developmental programming. Nanoparticle-linked drugs are emerging as a novel method to deliver therapeutics targeted to the placenta and avoid risking direct exposure to the fetus...
May 17, 2018: Pharmacological Research: the Official Journal of the Italian Pharmacological Society
https://www.readbyqxmd.com/read/29774505/mitigating-peroxynitrite-mediated-mitochondrial-dysfunction-in-aged-rat-brain-by-mitochondria-targeted-antioxidant-mitoq
#5
Arpan Kumar Maiti, B C Spoorthi, Nimai Chandra Saha, Ashis Kumar Panigrahi
Although reactive oxygen species mediated oxidative stress is a well-documented mechanism of aging, recent evidences indicate involvement of nitrosative stress in the same. As mitochondrial dysfunction is considered as one of the primary features of aging, the present study was designed to understand the involvement of nitrosative stress by studying the impact of a mitochondria-targeted antioxidant MitoQ, a peroxynitrite (ONOO- ) scavenger, on mitochondrial functions. Four groups of rats were included in this study: Group I: Young-6 months (-MitoQ), Group II: Aged-22 months (- MitoQ), Group III: Young-6 months (+ MitoQ), Group IV: Aged-22 months (+ MitoQ)...
May 17, 2018: Biogerontology
https://www.readbyqxmd.com/read/29758174/g-protein-coupled-estrogen-receptor-gper-deficiency-induces-cardiac-remodeling-through-oxidative-stress
#6
Hao Wang, Xuming Sun, Marina S Lin, Carlos M Ferrario, Holly Van Remmen, Leanne Groban
Oxidative stress has been implicated in the unfavorable changes in cardiac function and remodeling that occur after ovarian estrogen loss. Using ovariectomized rat models, we previously reported that the cardioprotective actions of estrogen are mediated by the G protein-coupled estrogen receptor (GPER). Here, in 9-month-old, female cardiomyocyte-specific GPER knockout (KO) mice vs sex- and age-matched wild-type (WT) mice, we found increased cardiac oxidative stress and oxidant damage, measured as a decreased ratio of reduced glutathione to oxidized glutathione, increased 4-hydroxynonenal and 8-hydroxy-2'-deoxyguanosine (8-oxo-DG) staining, and increased expression of oxidative stress-related genes...
April 25, 2018: Translational Research: the Journal of Laboratory and Clinical Medicine
https://www.readbyqxmd.com/read/29700332/mitoq-supplementation-prevent-long-term-impact-of-maternal-smoking-on-renal-development-oxidative-stress-and-mitochondrial-density-in-male-mice-offspring
#7
Suporn Sukjamnong, Yik Lung Chan, Razia Zakarya, Long The Nguyen, Ayad G Anwer, Amgad A Zaky, Rachana Santiyanont, Brian G Oliver, Ewa Goldys, Carol A Pollock, Hui Chen, Sonia Saad
To investigate the effect of maternal MitoQ treatment on renal disorders caused by maternal cigarette smoke exposure (SE). We have demonstrated that maternal SE during pregnancy increases the risk of developing chronic kidney disease (CKD) in adult offspring. Mitochondrial oxidative damage contributes to the adverse effects of maternal smoking on renal disorders. MitoQ is a mitochondria-targeted antioxidant that has been shown to protect against oxidative damage-related pathologies in many diseases. Female Balb/c mice (8 weeks) were divided into Sham (exposed to air), SE (exposed to cigarette smoke) and SEMQ (exposed to cigarette smoke with MitoQ supplemented from mating) groups...
April 26, 2018: Scientific Reports
https://www.readbyqxmd.com/read/29661838/chronic-supplementation-with-a-mitochondrial-antioxidant-mitoq-improves-vascular-function-in-healthy-older-adults
#8
Matthew J Rossman, Jessica R Santos-Parker, Chelsea A C Steward, Nina Z Bispham, Lauren M Cuevas, Hannah L Rosenberg, Kayla A Woodward, Michel Chonchol, Rachel A Gioscia-Ryan, Michael P Murphy, Douglas R Seals
Excess reactive oxygen species production by mitochondria is a key mechanism of age-related vascular dysfunction. Our laboratory has shown that supplementation with the mitochondrial-targeted antioxidant MitoQ improves vascular endothelial function by reducing mitochondrial reactive oxygen species and ameliorates arterial stiffening in old mice, but the effects in humans are unknown. Here, we sought to translate our preclinical findings to humans and determine the safety and efficacy of MitoQ. Twenty healthy older adults (60-79 years) with impaired endothelial function (brachial artery flow-mediated dilation <6%) underwent 6 weeks of oral supplementation with MitoQ (20 mg/d) or placebo in a randomized, placebo-controlled, double-blind, crossover design study...
June 2018: Hypertension
https://www.readbyqxmd.com/read/29642447/mitoq-loaded-chitosan-hyaluronan-composite-membranes-for-wound-healing
#9
Tamer M Tamer, Maurice N Collins, Katarina Valachová, Mohamed A Hassan, Ahmed M Omer, Mohamed S Mohy-Eldin, Karol Švík, Rastislav Jurčík, Ľubomír Ondruška, Csaba Biró, Ahmad B Albadarin, Ladislav Šoltés
Two self-associating biopolymers, namely chitosan (Ch) and a high-molar-mass hyaluronan (HA), were used to prepare membranes with the aim to protect and to enhance the healing of injured skin. A mitochondrially-targeted antioxidant-MitoQ-was incorporated into the mixture of biopolymers prior to their self-association. These three-component membranes were evaluated in detail utilising surface roughness measurements, contact angle measurements, hemocompatibility, and thrombogenicity analyses. Furthermore, in vivo application of Ch/HA/MitoQ membranes was assessed on injured rabbit and rat skin utilizing histological methods...
April 7, 2018: Materials
https://www.readbyqxmd.com/read/29611340/the-targeted-anti-oxidant-mitoq-causes-mitochondrial-swelling-and-depolarization-in-kidney-tissue
#10
Esther M Gottwald, Michael Duss, Milica Bugarski, Dominik Haenni, Claus D Schuh, Ehud M Landau, Andrew M Hall
Kidney proximal tubules (PTs) contain a high density of mitochondria, which are required to generate ATP to power solute transport. Mitochondrial dysfunction is implicated in the pathogenesis of numerous kidney diseases. Damaged mitochondria are thought to produce excess reactive oxygen species (ROS), which can lead to oxidative stress and activation of cell death pathways. MitoQ is a mitochondrial targeted anti-oxidant that has shown promise in preclinical models of renal diseases. However, recent studies in nonkidney cells have suggested that MitoQ might also have adverse effects...
April 2018: Physiological Reports
https://www.readbyqxmd.com/read/29540694/the-mitochondrially-targeted-antioxidant-mitoq-protects-the-intestinal-barrier-by-ameliorating-mitochondrial-dna-damage-via-the-nrf2-are-signaling-pathway
#11
Qiongyuan Hu, Jianan Ren, Guanwei Li, Jie Wu, Xiuwen Wu, Gefei Wang, Guosheng Gu, Huajian Ren, Zhiwu Hong, Jieshou Li
Disruption of the mucosal barrier following intestinal ischemia reperfusion (I/R) is life threatening in clinical practice. Mitochondrial dysfunction and oxidative stress significantly contribute to the early phase of I/R injury and amplify the inflammatory response. MitoQ is a mitochondrially targeted antioxidant that exerts protective effects following I/R injury. In the present study, we aimed to determine whether and how MitoQ protects intestinal epithelial cells (IECs) from I/R injury. In both in vivo and in vitro studies, we found that MitoQ pretreatment downregulated I/R-induced oxidative stress and stabilized the intestinal barrier, as evidenced by MitoQ-treated I/R mice exhibiting attenuated intestinal hyperpermeability, inflammatory response, epithelial apoptosis, and tight junction damage compared to controls...
March 14, 2018: Cell Death & Disease
https://www.readbyqxmd.com/read/29475133/reactive-oxygen-species-promote-tubular-injury-in-diabetic-nephropathy-the-role-of-the-mitochondrial-ros-txnip-nlrp3-biological-axis
#12
Yachun Han, Xiaoxuan Xu, Chengyuan Tang, Peng Gao, Xianghui Chen, Xiaofen Xiong, Ming Yang, Shikun Yang, Xuejing Zhu, Shuguang Yuan, Fuyou Liu, Li Xiao, Yashpal S Kanwar, Lin Sun
NLRP3/IL-1β activation via thioredoxin (TRX)/thioredoxin-interacting protein (TXNIP) following mitochondria ROS (mtROS) overproduction plays a key role in inflammation. However, the involvement of this process in tubular damage in the kidneys of patients with diabetic nephropathy (DN) is unclear. Here, we demonstrated that mtROS overproduction is accompanied by decreases in TRX expression and TXNIP up-regulation. In addition, we discovered that mtROS overproduction is also associated with increases in NLRP3/IL-1β and TGF-β expression in the kidneys of patients with DN and db/db mice...
June 2018: Redox Biology
https://www.readbyqxmd.com/read/29458285/induction-of-autophagy-by-depolarization-of-mitochondria
#13
Konstantin G Lyamzaev, Artem V Tokarchuk, Alisa A Panteleeva, Armen Y Mulkidjanian, Vladimir P Skulachev, Boris V Chernyak
Mitochondrial dysfunction plays a crucial role in the macroautophagy/autophagy cascade. In a recently published study Sun et al. described the induction of autophagy by the membranophilic triphenylphosphonium (TPP)-based cation 10-(6'-ubiquinonyl) decyltriphenylphosphonium (MitoQ) in HepG2 cells (Sun C, et al. "MitoQ regulates autophagy by inducing a pseudo-mitochondrial membrane potential [PMMP]", Autophagy 2017, 13:730-738.). Sun et al. suggested that MitoQ adsorbed to the inner mitochondrial membrane with its cationic moiety remaining in the intermembrane space, adding a large number of positive charges and establishing a "pseudo-mitochondrial membrane potential," which blocked the ATP synthase...
March 13, 2018: Autophagy
https://www.readbyqxmd.com/read/29452078/ice-free-cryopreservation-of-heart-valve-tissue-the-effect-of-adding-mitoq-to-a-vs83-formulation-and-its-influence-on-mitochondrial-dynamics
#14
Yulong Sui, Qing Fan, Bin Wang, Jixian Wang, Qing Chang
No abstract text is available yet for this article.
April 2018: Cryobiology
https://www.readbyqxmd.com/read/29421236/mitoq-improves-mitochondrial-dysfunction-in-heart-failure-induced-by-pressure-overload
#15
Rogério Faustino Ribeiro Junior, Erinne Rose Dabkowski, Kadambari Chandra Shekar, Kelly A O Connell, Peter A Hecker, Michael P Murphy
Heart failure remains a major public-health problem with an increase in the number of patients worsening from this disease. Despite current medical therapy, the condition still has a poor prognosis. Heart failure is complex but mitochondrial dysfunction seems to be an important target to improve cardiac function directly. Our goal was to analyze the effects of MitoQ (100 µM in drinking water) on the development and progression of heart failure induced by pressure overload after 14 weeks. The main findings are that pressure overload-induced heart failure in rats decreased cardiac function in vivo that was not altered by MitoQ...
March 2018: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/29419444/impact-of-the-mitochondria-targeted-antioxidant-mitoq-on-hypoxia-induced-pulmonary-hypertension
#16
Oleg Pak, Susan Scheibe, Azadeh Esfandiary, Mareike Gierhardt, Akylbek Sydykov, Angela Logan, Athanasios Fysikopoulos, Florian Veit, Matthias Hecker, Florian Kroschel, Karin Quanz, Alexandra Erb, Katharina Schäfer, Mirja Fassbinder, Nasim Alebrahimdehkordi, Hossein A Ghofrani, Ralph T Schermuly, Ralf P Brandes, Werner Seeger, Michael P Murphy, Norbert Weissmann, Natascha Sommer
Increased mitochondrial reactive oxygen species (ROS), particularly superoxide have been suggested to mediate hypoxic pulmonary vasoconstriction (HPV), chronic hypoxia-induced pulmonary hypertension (PH) and right ventricular (RV) remodelling.We determined ROS in acute, chronic hypoxia and investigated the effect of the mitochondria-targeted antioxidant MitoQ under these conditions.The effect of MitoQ or its inactive carrier substance, decyltriphenylphosphonium (TPP+ ), on acute HPV (1% O2 for 10 minutes) was investigated in isolated blood-free perfused mouse lungs...
February 1, 2018: European Respiratory Journal: Official Journal of the European Society for Clinical Respiratory Physiology
https://www.readbyqxmd.com/read/29388466/reactive-oxygen-species-induced-ca2-influx-via-trpv4-and-microvascular-endothelial-dysfunction-in-the-su5416-hypoxia-model-of-pulmonary-arterial-hypertension
#17
Karthik Suresh, Laura Servinsky, Haiyang Jiang, Zahna Bigham, Xin Yun, Corinne Kliment, John C Huetsch, Mahendra Damarla, Larissa A Shimoda
Pulmonary arterial hypertension (PAH) is a lethal disease characterized by elevations in pulmonary arterial pressure, in part due to formation of occlusive lesions in the distal arterioles of the lung. These complex lesions may comprise multiple cell types, including endothelial cells (ECs). To better understand the molecular mechanisms underlying EC dysfunction in PAH, lung microvascular endothelial cells (MVECs) were isolated from normoxic rats (N-MVEC) and rats subjected to SU5416 plus hypoxia (SuHx), an experimental model of PAH...
February 1, 2018: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/29378335/mitochondrial-rescue-prevents-glutathione-peroxidase-dependent-ferroptosis
#18
Anja Jelinek, Lukas Heyder, Michael Daude, Matthias Plessner, Sylvia Krippner, Robert Grosse, Wibke E Diederich, Carsten Culmsee
Research into oxidative cell death is producing exciting new mechanisms, such as ferroptosis, in the neuropathologies of cerebral ischemia and hemorrhagic brain insults. Ferroptosis is an oxidative form of regulated necrotic cell death featuring glutathione (GSH) depletion, disrupted glutathione peroxidase-4 (GPX4) redox defense and detrimental lipid reactive oxygen species (ROS) formation. Further, our recent findings identified mitochondrial damage in models of oxidative glutamate toxicity, glutathione peroxidase depletion, and ferroptosis...
March 2018: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/29317239/protective-effect-of-mitochondrial-targeted-antioxidant-mitoq-against-iron-ion-56-fe-radiation-induced-brain-injury-in-mice
#19
Lu Gan, Zhenhua Wang, Jing Si, Rong Zhou, Chao Sun, Yang Liu, Yancheng Ye, Yanshan Zhang, Zhiyuan Liu, Hong Zhang
Exposure to iron ion 56 Fe radiation (IR) during space missions poses a significant risk to the central nervous system and radiation exposure is intimately linked to the production of reactive oxygen species (ROS). MitoQ is a mitochondria-targeted antioxidant that has been shown to decrease oxidative damage and lower mitochondrial ROS in a number of animal models. Therefore, the present study aimed to investigate role of the mitochondrial targeted antioxidant MitoQ against 56 Fe particle irradiation-induced oxidative damage and mitochondria dysfunction in the mouse brains...
February 15, 2018: Toxicology and Applied Pharmacology
https://www.readbyqxmd.com/read/29289511/opening-of-voltage-dependent-anion-channels-promotes-reactive-oxygen-species-generation-mitochondrial-dysfunction-and-cell-death-in-cancer-cells
#20
David N DeHart, Diana Fang, Kareem Heslop, Li Li, John J Lemasters, Eduardo N Maldonado
Enhancement of aerobic glycolysis and suppression of mitochondrial metabolism characterize the pro-proliferative Warburg phenotype of cancer cells. High free tubulin in cancer cells closes voltage dependent anion channels (VDAC) to decrease mitochondrial membrane potential (ΔΨ), an effect antagonized by erastin, the canonical promotor of ferroptosis. Previously, we identified six compounds (X1-X6) that also block tubulin-dependent mitochondrial depolarization. Here, we hypothesized that VDAC opening after erastin and X1-X6 increases mitochondrial metabolism and reactive oxygen species (ROS) formation, leading to ROS-dependent mitochondrial dysfunction, bioenergetic failure and cell death...
February 2018: Biochemical Pharmacology
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