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Mitoq

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https://www.readbyqxmd.com/read/28121478/mitoq-regulates-autophagy-by-inducing-a-pseudo-mitochondrial-membrane-potential-pmmp
#1
Chao Sun, Xiongxiong Liu, Cuixia Di, Zhenhua Wang, Xiangquan Mi, Yang Liu, Qiuyue Zhao, Aihong Mao, Weiqiang Chen, Lu Gan, Hong Zhang
During the process of oxidative phosphorylation, protons are pumped into the mitochondrial intermembrane space to establish a mitochondrial membrane potential (MMP). The electrochemical gradient generated allows protons to return to the matrix through the ATP synthase complex and generates ATP in the process. MitoQ is a lipophilic cationic drug that is adsorbed to the inner mitochondrial membrane; however, the cationic moiety of MitoQ remains in the intermembrane space. We found that the positive charges in MitoQ inhibited the activity of respiratory chain complexes I, III, and IV, reduced proton production, and decreased oxygen consumption...
January 25, 2017: Autophagy
https://www.readbyqxmd.com/read/28050775/neuroprotective-efficacy-of-mitochondrial-antioxidant-mitoq-in-suppressing-peroxynitrite-mediated-mitochondrial-dysfunction-inflicted-by-lead-toxicity-in-the-rat-brain
#2
Arpan Kumar Maiti, Nimai Chandra Saha, Sunil S More, Ashish Kumar Panigrahi, Goutam Paul
Lead (Pb) is one of the most pollutant metals that accumulate in the brain mitochondria disrupting mitochondrial structure and function. Though oxidative stress mediated by reactive oxygen species remains the most accepted mechanism of Pb neurotoxicity, some reports suggest the involvement of nitric oxide ((•)NO) and reactive nitrogen species in Pb-induced neurotoxicity. But the impact of Pb neurotoxicity on mitochondrial respiratory enzyme complexes remains unknown with no relevant report highlighting the involvement of peroxynitrite (ONOO(-)) in it...
January 3, 2017: Neurotoxicity Research
https://www.readbyqxmd.com/read/28034666/oxidative-stress-in-sepsis-pathophysiological-implications-justifying-antioxidant-co-therapy
#3
REVIEW
Carlos André Prauchner
Sepsis is one of the main causes of death among critically ill patients. Sepsis pathogenesis includes infection by gram-negative and gram-positive bacteria, fungi, or both; exacerbated inflammatory response; hypotension, with potential to cause vasodilatory shock; and lesser delivery of oxygen to tissues due to impairment of oxygen utilization by cells. The participation of reactive species and/or free radicals such as nitric oxide (NO), peroxynitrite (ONOO(-)), superoxide (O2(-)), hydrogen peroxide (H2O2), and hydroxyl radical (OH) has been reported to underlie these effects...
December 26, 2016: Burns: Journal of the International Society for Burn Injuries
https://www.readbyqxmd.com/read/28033563/the-mitochondria-targeted-antioxidant-mitoq-ameliorated-tubular-injury-mediated-by-mitophagy-in-diabetic-kidney-disease-via-nrf2-pink1
#4
Li Xiao, Xiaoxuan Xu, Fan Zhang, Ming Wang, Yan Xu, Dan Tang, Jiahui Wang, Yan Qin, Yu Liu, Chengyuan Tang, Liyu He, Anna Greka, Zhiguang Zhou, Fuyou Liu, Zheng Dong, Lin Sun
Mitochondria play a crucial role in tubular injury in diabetic kidney disease (DKD). MitoQ is a mitochondria-targeted antioxidant that exerts protective effects in diabetic mice, but the mechanism underlying these effects is not clear. We demonstrated that mitochondrial abnormalities, such as defective mitophagy, mitochondrial reactive oxygen species (ROS) overexpression and mitochondrial fragmentation, occurred in the tubular cells of db/db mice, accompanied by reduced PINK and Parkin expression and increased apoptosis...
December 21, 2016: Redox Biology
https://www.readbyqxmd.com/read/28030582/therapeutic-targeting-of-the-mitochondria-initiates-excessive-superoxide-production-and-mitochondrial-depolarization-causing-decreased-mtdna-integrity
#5
Kaytee L Pokrzywinski, Thomas G Biel, Dmitry Kryndushkin, V Ashutosh Rao
Mitochondrial dysregulation is closely associated with excessive reactive oxygen species (ROS) production. Altered redox homeostasis has been implicated in the onset of several diseases including cancer. Mitochondrial DNA (mtDNA) and proteins are particularly sensitive to ROS as they are in close proximity to the respiratory chain (RC). Mitoquinone (MitoQ), a mitochondria-targeted redox agent, selectively damages breast cancer cells possibly through damage induced via enhanced ROS production. However, the effects of MitoQ and other triphenylphosphonium (TPP+) conjugated agents on cancer mitochondrial homeostasis remain unknown...
2016: PloS One
https://www.readbyqxmd.com/read/27930931/deficiency-in-duox2-activity-alleviates-ileitis-in-gpx1-and-gpx2-knockout-mice-without-affecting-apoptosis-incidence-in-the-crypt-epithelium
#6
Fong-Fong Chu, R Steven Esworthy, James H Doroshow, Helmut Grasberger, Agnes Donko, Thomas L Leto, Qiang Gao, Binghui Shen
Mice deficient in glutathione peroxidase (GPx)-1 and -2 (GPx1(-/-)GPx2(-/-) double knockout or DKO mice) develop very-early-onset (VEO) ileocolitis, suggesting that lack of defense against reactive oxygen species (ROS) renders susceptibility to intestinal inflammation. Two members of ROS-generating NADPH oxidase family, NOX1 and DUOX2, are highly inducible in the intestinal epithelium. Previously, we reported that Nox1 deficiency ameliorated the pathology in DKO mice (Nox1-TKO). The role of Duox2 in ileocolitis of the DKO mice is evaluated here in Duoxa-TKO mice by breeding DKO mice with Duoxa(-/-) mice (Duoxa-TKO), which do not have Duox2 activity...
November 22, 2016: Redox Biology
https://www.readbyqxmd.com/read/27922686/necrox-5-prevents-breast-cancer-metastasis-by-akt-inhibition-via-reducing-intracellular-calcium-levels
#7
Jin-Hee Park, Hyoung Kyu Kim, Hana Jung, Ki Hyang Kim, Mi Seon Kang, Jun Hyuk Hong, Byeng Chul Yu, Sungjae Park, Su-Kil Seo, Il Whan Choi, Soon Ha Kim, Nari Kim, Jin Han, Sae Gwang Park
A major goal of breast cancer research is to prevent the molecular events that lead to tumour metastasis. It is well-established that both cytoplasmic and mitochondrial reactive oxygen species (ROS) play important roles in cell migration and metastasis. Accordingly, this study examined the molecular mechanisms of the anti-metastatic effects of NecroX-5, a mitochondrial ROS scavenger. NecroX-5 inhibited lung cancer metastasis by ameliorating migration in a mouse model. In human cancer cells, the inhibition of migration by NecroX-5 is cell type-dependent...
January 2017: International Journal of Oncology
https://www.readbyqxmd.com/read/27911703/understanding-and-preventing-mitochondrial-oxidative-damage
#8
REVIEW
Michael P Murphy
Mitochondrial oxidative damage has long been known to contribute to damage in conditions such as ischaemia-reperfusion (IR) injury in heart attack. Over the past years, we have developed a series of mitochondria-targeted compounds designed to ameliorate or determine how this damage occurs. I will outline some of this work, from MitoQ to the mitochondria-targeted S-nitrosating agent, called MitoSNO, that we showed was effective in preventing reactive oxygen species (ROS) formation in IR injury with therapeutic implications...
October 15, 2016: Biochemical Society Transactions
https://www.readbyqxmd.com/read/27899525/reactive-oxygen-species-induce-virus-independent-mavs-oligomerization-in-systemic-lupus-erythematosus
#9
Iwona A Buskiewicz, Theresa Montgomery, Elizabeth C Yasewicz, Sally A Huber, Michael P Murphy, Richard C Hartley, Ryan Kelly, Mary K Crow, Andras Perl, Ralph C Budd, Andreas Koenig
The increased expression of genes induced by type I interferon (IFN) is characteristic of viral infections and systemic lupus erythematosus (SLE). We showed that mitochondrial antiviral signaling (MAVS) protein, which normally forms a complex with retinoic acid gene I (RIG-I)-like helicases during viral infection, was activated by oxidative stress independently of RIG-I helicases. We found that chemically generated oxidative stress stimulated the formation of MAVS oligomers, which led to mitochondrial hyperpolarization and decreased adenosine triphosphate production and spare respiratory capacity, responses that were not observed in similarly treated cells lacking MAVS...
November 29, 2016: Science Signaling
https://www.readbyqxmd.com/read/27875805/voluntary-aerobic-exercise-increases-arterial-resilience-and-mitochondrial-health-with-aging-in-mice
#10
Rachel A Gioscia-Ryan, Micah L Battson, Lauren M Cuevas, Melanie C Zigler, Amy L Sindler, Douglas R Seals
Mitochondrial dysregulation and associated excessive reactive oxygen species (mtROS) production is a key source of oxidative stress in aging arteries that reduces baseline function and may influence resilience (ability to withstand stress). We hypothesized that voluntary aerobic exercise would increase arterial resilience in old mice. An acute mitochondrial stressor (rotenone) caused greater (further) impairment in peak carotid EDD in old (~27 mo., OC, n=12; -32.5±-10.5%) versus young (~7 mo., YC n=11; -5...
November 22, 2016: Aging
https://www.readbyqxmd.com/read/27810734/the-mitochondria-targeted-antioxidant-mitoq-modulates-oxidative-stress-inflammation-and-leukocyte-endothelium-interactions-in-leukocytes-isolated-from-type-2-diabetic-patients
#11
Irene Escribano-Lopez, Noelia Diaz-Morales, Susana Rovira-Llopis, Arantxa Martinez de Marañon, Samuel Orden, Angeles Alvarez, Celia Bañuls, Milagros Rocha, Michael P Murphy, Antonio Hernandez-Mijares, Victor M Victor
It is not known if the mitochondria-targeted antioxidants such as mitoquinone (MitoQ) can modulate oxidative stress and leukocyte-endothelium interactions in T2D patients. We aimed to evaluate the beneficial effect of MitoQ on oxidative stress parameters and leukocyte-endothelium interactions in leukocytes of T2D patients. The study population consisted of 98 T2D patients and 71 control subjects. We assessed metabolic and anthropometric parameters, mitochondrial reactive oxygen species (ROS) production, glutathione peroxidase 1 (GPX-1), NFκB-p65, TNFα and leukocyte-endothelium interactions...
October 27, 2016: Redox Biology
https://www.readbyqxmd.com/read/27659264/cellular-and-molecular-mechanisms-of-action-of-mitochondria-targeted-antioxidants
#12
Boris A Feniouk, Vladimir P Skulachev
Reactive oxygen species generated in mitochondria is an important factor contributing to mitochondrial and cellular dysfunction underlying many degenerative diseases, chronic pathologies and aging. The idea of delivering antioxidant molecules to mitochondria in vivo to treat these diseases and slow aging intensively developed in the last 20 years. Derivatives of quinones covalently conjugated to a lipophilic cation (e.g., MitoQ and SkQ) were the most extensively studied mitochondria-targeted antioxidants. These compounds have now been used in a wide range of in vitro and in vivo studies, as well as in clinical trials in humans...
September 21, 2016: Current Aging Science
https://www.readbyqxmd.com/read/27549376/targeting-mitochondria-in-cardiovascular-diseases
#13
Filomena S G Silva, Rui F Simões, Renata Couto, Paulo J Oliveira
BACKGROUND: Cardiovascular diseases (CVDs) are one of the main factors responsible for human morbidity and mortality. Since mitochondria play a critical role in the regulation of cardiac tissue homeostasis, this organelle is a critical target for the protective effects of several pharmaceuticals. Although specific mitochondria-targeted antioxidants and some pharmacological agents are described as potential cardioprotective agents, there are still a few effective mitochondrial therapies for the treatment of CVDs...
August 22, 2016: Current Pharmaceutical Design
https://www.readbyqxmd.com/read/27501153/mitochondria-specific-antioxidant-supplementation-does-not-influence-endurance-exercise-training-induced-adaptations-in-circulating-angiogenic-cells-skeletal-muscle-oxidative-capacity-or-maximal-oxygen-uptake
#14
Daniel D Shill, W Michael Southern, T Bradley Willingham, Kasey A Lansford, Kevin K McCully, Nathan T Jenkins
KEY POINTS: Reducing excessive oxidative stress, through chronic exercise or antioxidants, can decrease the negative effects induced by excessive amounts of oxidative stress. Transient increases in oxidative stress produced during acute exercise facilitate beneficial vascular training adaptations, but the effects of non-specific antioxidants on exercise training-induced vascular adaptations remain elusive. Circulating angiogenic cells (CACs) are an exercise-inducible subset of white blood cells that maintain vascular integrity...
December 1, 2016: Journal of Physiology
https://www.readbyqxmd.com/read/27394174/mitochondrial-impairments-contribute-to-spinocerebellar-ataxia-type-1-progression-and-can-be-ameliorated-by-the-mitochondria-targeted-antioxidant-mitoq
#15
David M Stucki, Céline Ruegsegger, Silvio Steiner, Julika Radecke, Michael P Murphy, Benoît Zuber, Smita Saxena
Spinocerebellar ataxia type 1 (SCA1), due to an unstable polyglutamine expansion within the ubiquitously expressed Ataxin-1 protein, leads to the premature degeneration of Purkinje cells (PCs), decreasing motor coordination and causing death within 10-15 years of diagnosis. Currently, there are no therapies available to slow down disease progression. As secondary cellular impairments contributing to SCA1 progression are poorly understood, here, we focused on identifying those processes by performing a PC specific proteome profiling of Sca1(154Q/2Q) mice at a symptomatic stage...
August 2016: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/27313826/mitochondria-targeted-antioxidants-future-perspectives-in-kidney-ischemia-reperfusion-injury
#16
REVIEW
Aleksandra Kezic, Ivan Spasojevic, Visnja Lezaic, Milica Bajcetic
Kidney ischemia/reperfusion injury emerges in various clinical settings as a great problem complicating the course and outcome. Ischemia/reperfusion injury is still an unsolved puzzle with a great diversity of investigational approaches, putting the focus on oxidative stress and mitochondria. Mitochondria are both sources and targets of ROS. They participate in initiation and progression of kidney ischemia/reperfusion injury linking oxidative stress, inflammation, and cell death. The dependence of kidney proximal tubule cells on oxidative mitochondrial metabolism makes them particularly prone to harmful effects of mitochondrial damage...
2016: Oxidative Medicine and Cellular Longevity
https://www.readbyqxmd.com/read/27226607/the-activity-of-menkes-disease-protein-atp7a-is-essential-for-redox-balance-in-mitochondria
#17
Ashima Bhattacharjee, Haojun Yang, Megan Duffy, Emily Robinson, Arianrhod Conrad-Antoville, Ya-Wen Lu, Tony Capps, Lelita Braiterman, Michael Wolfgang, Michael P Murphy, Ling Yi, Stephen G Kaler, Svetlana Lutsenko, Martina Ralle
Copper-transporting ATPase ATP7A is essential for mammalian copper homeostasis. Loss of ATP7A activity is associated with fatal Menkes disease and various other pathologies. In cells, ATP7A inactivation disrupts copper transport from the cytosol into the secretory pathway. Using fibroblasts from Menkes disease patients and mouse 3T3-L1 cells with a CRISPR/Cas9-inactivated ATP7A, we demonstrate that ATP7A dysfunction is also damaging to mitochondrial redox balance. In these cells, copper accumulates in nuclei, cytosol, and mitochondria, causing distinct changes in their redox environment...
August 5, 2016: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/27186319/the-mitochondria-targeted-antioxidant-mitoq-attenuates-liver-fibrosis-in-mice
#18
Hasibur Rehman, Qinlong Liu, Yasodha Krishnasamy, Zengdun Shi, Venkat K Ramshesh, Khujista Haque, Rick G Schnellmann, Michael P Murphy, John J Lemasters, Don C Rockey, Zhi Zhong
Oxidative stress plays an essential role in liver fibrosis. This study investigated whether MitoQ, an orally active mitochondrial antioxidant, decreases liver fibrosis. Mice were injected with corn oil or carbon tetrachloride (CCl4, 1:3 dilution in corn oil; 1 µl/g, ip) once every 3 days for up to 6 weeks. 4-Hydroxynonenal adducts increased markedly after CCl4 treatment, indicating oxidative stress. MitoQ attenuated oxidative stress after CCl4. Collagen 1α1 mRNA and hydroxyproline increased markedly after CCl4 treatment, indicating increased collagen formation and deposition...
2016: International Journal of Physiology, Pathophysiology and Pharmacology
https://www.readbyqxmd.com/read/27182824/ubiquinol-and-plastoquinol-triphenylphosphonium-conjugates-can-carry-electrons-through-phospholipid-membranes
#19
Tatyana I Rokitskaya, Michael P Murphy, Vladimir P Skulachev, Yuri N Antonenko
Many mitochondria-targeted antioxidants (MTAs) that comprise a quinol moiety covalently attached through an aliphatic carbon chain to the lipophilic triphenylphosphonium cation are widely used for evaluating the role of mitochondria in pathological processes involving oxidative stress. The potency of MTAs to carry electrons across biological membranes and thereby mediate transmembrane redox processes was unknown. To assess this, we measured the rate of ferricyanide reduction inside liposomes by external ascorbate...
October 2016: Bioelectrochemistry
https://www.readbyqxmd.com/read/27172658/-mitochondria-targeted-antioxidant-mitoquinone-protects-post-thaw-human-sperm-against-oxidative-stress-injury
#20
Li Liu, Mei-jiao Wang, Ting-he Yu, Zhi Cheng, Min Li, Qian-wen Guo
OBJECTIVE: To investigate the potential protective effect of the mitochondria-targeted antioxidant Mitoquinone (MitoQ) on post-thaw human sperm. METHODS: Semen samples were collected from 60 normal fertile men, each divided into six parts of equal volume to be incubated at 37 °C in normal saline (G0, control) or in the extender with 2 nmol/L (G1), 20 nmol/L (G2), 200 nmol/L (G3), 2 µmol/L (G4), and 20 µmol/L of MitoQ (G5). After one hour of incubation, the samples were subjected to computer-assisted semen analysis (CASA) for sperm motility, flow cytometry for reactive oxygen species (ROS), thiobarbituric acid assay for the concentration of malondialdehyde (MDA), and MitoTracker fluorescent staining and flow cytometry for the sperm mitochondrial membrane potential (MMP)...
March 2016: Zhonghua Nan Ke Xue, National Journal of Andrology
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