Journal ArticleDOI
Metformin prevents ischemia reperfusion-induced oxidative stress in the fatty liver by attenuation of reactive oxygen species formation
Monika Cahova,Eliska Palenickova,Helena Dankova,Eva Sticova,Martin Burian,Zdenek Drahota,Zuzana Červinková,Otto Kucera,Christina Gladkova,Pavel Stopka,Jana Krizova,Zuzana Papackova,Olena Oliyarnyk,Ludmila Kazdova +13 more
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TLDR
It is proposed that the beneficial effect of metformin action is based on a combination of three contributory mechanisms: increased antioxidant enzyme activity, lower mitochondrial ROS production, and reduction of postischemic inflammation.Abstract:
Nonalcoholic fatty liver disease is associated with chronic oxidative stress. In our study, we explored the antioxidant effect of antidiabetic metformin on chronic [high-fat diet (HFD)-induced] and...read more
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A Unifying Mechanism for Mitochondrial Superoxide Production during Ischemia-Reperfusion Injury.
Edward T. Chouchani,Victoria R. Pell,Andrew M. James,Lorraine M. Work,Kourosh Saeb-Parsy,Christian Frezza,Thomas Krieg,Michael P. Murphy +7 more
TL;DR: The metabolic factors underlying IR injury are surveyed and a unifying mechanism for its causes is proposed that makes sense of the huge amount of disparate data in this area and provides testable hypotheses and new directions for therapies.
Journal ArticleDOI
Oxidative stress during acetaminophen hepatotoxicity: Sources, pathophysiological role and therapeutic potential.
TL;DR: It is suggested that mitochondrial targeted antioxidants can be viable therapeutic agents against hepatotoxicity induced by APAP overdose, and re-purposing existing drugs to target oxidative stress and other concurrent signaling events can be a promising strategy to increase its potential application in patients with AP AP overdose.
Journal Article
Mitochondrial Electron Transport Complex I Is a Potential Source of Oxygen Free Radicals in the Failing Myocardium
TomomiIde,HiroyukiTsutsui,ShintaroKinugawa,HideoUtsumi,DongchonKang,NobutakaHattori,KojiUchida,Ken-ichiArimura,KensukeEgashira,AkiraTakeshita +9 more
TL;DR: The amount of thiobarbituric acid reactive substances increased in the canine HF hearts subjected to rapid ventricular pacing for 4 weeks, and immunohistochemical staining of 4-hydroxy-2-nonenal ROS-induced lipid peroxides was detected in cardiac myocytes but not in interstitial cells of HF animals.
Journal ArticleDOI
Mitochondria and cardiovascular diseases-from pathophysiology to treatment.
Gerasimos Siasos,Vasiliki Tsigkou,Marinos Kosmopoulos,Dimosthenis G Theodosiadis,Spyridon Simantiris,Nikoletta Maria Tagkou,Athina Tsimpiktsioglou,Panagiota K. Stampouloglou,Evangelos Oikonomou,Konstantinos Mourouzis,Anastasios Philippou,Manolis Vavuranakis,Christodoulos Stefanadis,Dimitris Tousoulis,Athanasios G. Papavassiliou +14 more
TL;DR: The aim of future research is to design molecules which selectively target mitochondrial dysfunction and restore the capacity of cellular anti-oxidant enzymes.
Journal ArticleDOI
Metformin-Induced Mitochondrial Complex I Inhibition: Facts, Uncertainties, and Consequences.
TL;DR: A brief review attempts to gather arguments for and against each hypothesis concerning the mechanism by which metformin inhibits Complex I and to highlight remaining questions about the toxicity mechanism of meetformin for certain cancer cells.
References
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Journal ArticleDOI
Biochemistry and molecular cell biology of diabetic complications
TL;DR: This integrating paradigm provides a new conceptual framework for future research and drug discovery in diabetes-specific microvascular disease and seems to reflect a single hyperglycaemia-induced process of overproduction of superoxide by the mitochondrial electron-transport chain.
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How mitochondria produce reactive oxygen species.
TL;DR: The description outlined here facilitates the understanding of factors that favour mitochondrial ROS production and develops better methods to measure mitochondrial O2•− and H2O2 formation in vivo, as uncertainty about these values hampers studies on the role of mitochondrial ROS in pathological oxidative damage and redox signalling.
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Reactive Oxygen Species Promote TNFα-Induced Death and Sustained JNK Activation by Inhibiting MAP Kinase Phosphatases
TL;DR: It is shown that TNFalpha-induced ROS, whose accumulation is suppressed by mitochondrial superoxide dismutase, cause oxidation and inhibition of JNK-inactivating phosphatases by converting their catalytic cysteine to sulfenic acid, which results in sustained JNK activation, which is required for cytochrome c release and caspase 3 cleavage.
Journal ArticleDOI
Biochemical and molecular investigations in respiratory chain deficiencies
Pierre Rustin,Dominique Chretien,Thomas Bourgeron,Bénédicte Gérard,Agnès Rötig,Jean-Marie Saudubray,Arnold Munnich +6 more
TL;DR: This paper describes the present strategy for the investigation of respiratory chain disorders in humans and describes biochemical and molecular methods, allowing investigation in both adults and young children.
Journal ArticleDOI
Metformin inhibits hepatic gluconeogenesis in mice independently of the LKB1/AMPK pathway via a decrease in hepatic energy state
Marc Foretz,Sophie Hébrard,Jocelyne Leclerc,Elham Zarrinpashneh,Maud Soty,Gilles Mithieux,Kei Sakamoto,Fabrizio Andreelli,Benoit Viollet +8 more
TL;DR: It is found that in mice lacking AMPK in the liver, blood glucose levels were comparable to those in wild-type mice, and the hypoglycemic effect of metformin was maintained, demonstrating that met formin inhibits hepatic gluconeogenesis in an LKB1- and AMPK-independent manner via a decrease in hepatic energy state.