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  1. Article ; Online: Calorie restriction changes lipidomic profiles and maintains mitochondrial function and redox balance during isoproterenol-induced cardiac hypertrophy.

    David, Cícera Edna Barbosa / Lucas, Aline Maria Brito / Cunha, Pedro Lourenzo Oliveira / Viana, Yuana Ivia Ponte / Yoshinaga, Marcos Yukio / Miyamoto, Sayuri / Filho, Adriano Brito Chaves / Varela, Anna Lídia Nunes / Kowaltowski, Alicia Juliana / Facundo, Heberty Tarso

    Journal of physiology and biochemistry

    2022  Volume 78, Issue 1, Page(s) 283–294

    Abstract: Typically, healthy cardiac tissue utilizes more fat than any other organ. Cardiac hypertrophy induces a metabolic shift leading to a preferential consumption of glucose over fatty acids to support the high energetic demand. Calorie restriction is a ... ...

    Abstract Typically, healthy cardiac tissue utilizes more fat than any other organ. Cardiac hypertrophy induces a metabolic shift leading to a preferential consumption of glucose over fatty acids to support the high energetic demand. Calorie restriction is a dietary procedure that induces health benefits and lifespan extension in many organisms. Given the beneficial effects of calorie restriction, we hypothesized that calorie restriction prevents cardiac hypertrophy, lipid content changes, mitochondrial and redox dysregulation. Strikingly, calorie restriction reversed isoproterenol-induced cardiac hypertrophy. Isolated mitochondria from hypertrophic hearts produced significantly higher levels of succinate-driven H
    MeSH term(s) Caloric Restriction ; Cardiomegaly/chemically induced ; Cardiomegaly/drug therapy ; Cardiomegaly/prevention & control ; Humans ; Hydrogen Peroxide/metabolism ; Isoproterenol/metabolism ; Isoproterenol/toxicity ; Lipidomics ; Mitochondria/metabolism ; Oxidation-Reduction ; Oxidative Stress
    Chemical Substances Hydrogen Peroxide (BBX060AN9V) ; Isoproterenol (L628TT009W)
    Language English
    Publishing date 2022-01-13
    Publishing country Spain
    Document type Journal Article
    ZDB-ID 1325104-1
    ISSN 1877-8755 ; 0034-9402 ; 1138-7548
    ISSN (online) 1877-8755
    ISSN 0034-9402 ; 1138-7548
    DOI 10.1007/s13105-021-00863-4
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.B 198: Show issues Location:
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    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

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  2. Article ; Online: Quercetin treatment increases H

    de Lacerda Alexandre, Joana Varlla / Viana, Yuana Ivia Ponte / David, Cícera Edna Barbosa / Cunha, Pedro Lourenzo Oliveira / Albuquerque, Amanda Cabral / Varela, Anna Lídia Nunes / Kowaltowski, Alicia J / Facundo, Heberty Tarso

    Naunyn-Schmiedeberg's archives of pharmacology

    2020  Volume 394, Issue 2, Page(s) 217–226

    Abstract: Oxidative stress, characterized by the accumulation of reactive oxygen species (ROS), is implicated in the pathogenesis of several diseases, including cardiac hypertrophy. The flavonoid quercetin is a potent ROS scavenger, with several beneficial effects ...

    Abstract Oxidative stress, characterized by the accumulation of reactive oxygen species (ROS), is implicated in the pathogenesis of several diseases, including cardiac hypertrophy. The flavonoid quercetin is a potent ROS scavenger, with several beneficial effects for the cardiovascular system, including antihypertrophic effects. Oxidative imbalance has been implicated in cardiac hypertrophy and heart failure. In this work, we tested whether quercetin could attenuate cardiac hypertrophy by improving redox balance and mitochondrial homeostasis. To test this hypothesis, we treated a group of mice with isoproterenol (30 mg/kg/day) for 4 or 8 consecutive days. Another group received quercetin (10 mg/kg/day) from day 5th of isoproterenol treatment. We carried out the following assays in cardiac tissue: measurement of cardiac hypertrophy, protein sulfhydryl, catalase, Cu/Zn and Mn-superoxide dismutase (SOD) activity, detection of H
    MeSH term(s) Animals ; Antioxidants/pharmacology ; Antioxidants/therapeutic use ; Cardiomegaly/chemically induced ; Cardiomegaly/drug therapy ; Cardiomegaly/metabolism ; Catalase/metabolism ; Hydrogen Peroxide/metabolism ; Isoproterenol ; Male ; Mice ; Mitochondria/drug effects ; Mitochondria/metabolism ; Myocardium/metabolism ; Quercetin/pharmacology ; Quercetin/therapeutic use ; Superoxide Dismutase/metabolism
    Chemical Substances Antioxidants ; Quercetin (9IKM0I5T1E) ; Hydrogen Peroxide (BBX060AN9V) ; Catalase (EC 1.11.1.6) ; Superoxide Dismutase (EC 1.15.1.1) ; Isoproterenol (L628TT009W)
    Language English
    Publishing date 2020-09-15
    Publishing country Germany
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 121471-8
    ISSN 1432-1912 ; 0028-1298
    ISSN (online) 1432-1912
    ISSN 0028-1298
    DOI 10.1007/s00210-020-01953-8
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Ud II Zs.5: Show issues Location:
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  3. Article ; Online: Diazoxide Modulates Cardiac Hypertrophy by Targeting H2O2 Generation and Mitochondrial Superoxide Dismutase Activity.

    Lucas, Aline Maria Brito / de Lacerda Alexandre, Joana Varlla / Araújo, Maria Thalyne Silva / David, Cicera Edna Barbosa / Ponte Viana, Yuana Ivia / Coelho, Beatriz Neves / Caldas, Francisco Rodrigo Lemos / Varela, Anna Lídia Nunes / Kowaltowski, Alicia Juliana / Facundo, Heberty Tarso

    Current molecular pharmacology

    2019  Volume 13, Issue 1, Page(s) 76–83

    Abstract: Background: Cardiac hypertrophy involves marked wall thickening or chamber enlargement. If sustained, this condition will lead to dysfunctional mitochondria and oxidative stress. Mitochondria have ATP-sensitive K+ channels (mitoKATP) in the inner ... ...

    Abstract Background: Cardiac hypertrophy involves marked wall thickening or chamber enlargement. If sustained, this condition will lead to dysfunctional mitochondria and oxidative stress. Mitochondria have ATP-sensitive K+ channels (mitoKATP) in the inner membrane that modulate the redox status of the cell.
    Objective: We investigated the in vivo effects of mitoKATP opening on oxidative stress in isoproterenol- induced cardiac hypertrophy.
    Methods: Cardiac hypertrophy was induced in Swiss mice treated intraperitoneally with isoproterenol (ISO - 30 mg/kg/day) for 8 days. From day 4, diazoxide (DZX - 5 mg/kg/day) was used in order to open mitoKATP (a clinically relevant therapy scheme) and 5-hydroxydecanoate (5HD - 5 mg/kg/day) or glibenclamide (GLI - 3 mg/kg/day) were used as mitoKATP blockers.
    Results: Isoproterenol-treated mice had elevated heart weight/tibia length ratios (HW/TL). Additionally, hypertrophic hearts had elevated levels of carbonylated proteins and Thiobarbituric Acid Reactive Substances (TBARS), markers of protein and lipid oxidation. In contrast, mitoKATP opening with DZX avoided ISO effects on gross hypertrophic markers (HW/TL), carbonylated proteins and TBARS, in a manner reversed by 5HD and GLI. Moreover, DZX improved mitochondrial superoxide dismutase activity. This effect was also blocked by 5HD and GLI. Additionally, ex vivo treatment of isoproterenol- induced hypertrophic cardiac tissue with DZX decreased H2O2 production in a manner sensitive to 5HD, indicating that this drug also acutely avoids oxidative stress.
    Conclusion: Our results suggest that diazoxide blocks oxidative stress and reverses cardiac hypertrophy. This pharmacological intervention could be a potential therapeutic strategy to prevent oxidative stress associated with cardiac hypertrophy.
    MeSH term(s) Animals ; Cardiomegaly/chemically induced ; Cardiomegaly/drug therapy ; Cardiomegaly/metabolism ; Diazoxide/pharmacology ; Diazoxide/therapeutic use ; Drug Evaluation, Preclinical ; Hydrogen Peroxide/metabolism ; Ion Transport/drug effects ; Isoproterenol/toxicity ; Mice ; Oxidative Stress/drug effects ; Potassium/metabolism ; Potassium Channels/drug effects ; Protein Carbonylation/drug effects ; Superoxide Dismutase/metabolism ; Thiobarbituric Acid Reactive Substances/analysis
    Chemical Substances Potassium Channels ; Thiobarbituric Acid Reactive Substances ; mitochondrial K(ATP) channel ; Hydrogen Peroxide (BBX060AN9V) ; Superoxide Dismutase (EC 1.15.1.1) ; superoxide dismutase 2 (EC 1.15.1.1) ; Isoproterenol (L628TT009W) ; Diazoxide (O5CB12L4FN) ; Potassium (RWP5GA015D)
    Language English
    Publishing date 2019-07-25
    Publishing country United Arab Emirates
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 1874-4702
    ISSN (online) 1874-4702
    DOI 10.2174/1874467212666190723144006
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: Calorie restriction attenuates hypertrophy-induced redox imbalance and mitochondrial ATP-sensitive K+ channel repression

    David, Cicera Edna Barbosa / Aline Maria Brito Lucas / Maria Thalyne Silva Araújo / Beatriz Neves Coelho / Juarez Braga Soares Neto / Bruna Raysa Campos Portela / Anna Lídia Nunes Varela / Alicia J. Kowaltowski / Heberty T. Facundo

    Journal of nutritional biochemistry. 2018 Dec., v. 62

    2018  

    Abstract: Oxidative stress has been implicated in the pathogenesis of cardiac hypertrophy and associated heart failure. Cardiac tissue grows in response to pressure or volume overload, leading to wall thickening or chamber enlargement. If sustained, this condition ...

    Abstract Oxidative stress has been implicated in the pathogenesis of cardiac hypertrophy and associated heart failure. Cardiac tissue grows in response to pressure or volume overload, leading to wall thickening or chamber enlargement. If sustained, this condition will lead to a dysfunctional cardiac tissue and oxidative stress. Calorie restriction (CR) is a powerful intervention to improve health and delay aging. Here, we investigated whether calorie restriction in mice prevented isoproterenol-induced cardiac hypertrophy in vivo by avoiding reactive oxygen species (ROS) production and maintaining antioxidant enzymatic activity. Additionally, we investigated the involvement of mitochondrial ATP-sensitive K+ channels (mitoKATP) in cardiac hypertrophy. CR was induced by 40% reduction in daily calorie ingestion. After 3 weeks on CR or ad libitum (Control) feeding, Swiss mice were treated intraperitoneally with isoproterenol (30 mg/kg per day) for 8 days to induce hypertrophy. Isoproterenol-treated mice had elevated heart weight/tibia length ratios and cardiac protein levels. These gross hypertrophic markers were significantly reduced in CR mice. Cardiac tissue from isoproterenol-treated CR mice also produced less H2O2 and had lower protein sulfydryl oxidation. Additionally, calorie restriction blocked hypertrophic-induced antioxidant enzyme (catalase, superoxide dismutase and glutathione peroxidase) activity repression during cardiac hypertrophy. MitoKATP opening was repressed in isolated mitochondria from hypertrophic hearts, in a manner sensitive to calorie restriction. Finally, mitoKATP inhibition significantly blocked the protective effects of calorie restriction. Altogether, our results suggest that CR improves intracellular redox balance during cardiac hypertrophy and prevents this process in a mechanism involving mitoKATP activation.
    Keywords catalase ; enzyme activity ; glutathione peroxidase ; heart ; heart failure ; hydrogen peroxide ; hypertrophy ; ingestion ; isoproterenols ; laboratory animals ; low calorie diet ; mice ; mitochondria ; oxidation ; oxidative stress ; pathogenesis ; potassium channels ; protective effect ; protein content ; superoxide dismutase ; tibia
    Language English
    Dates of publication 2018-12
    Size p. 87-94.
    Publishing place Elsevier Inc.
    Document type Article
    ZDB-ID 1014929-6
    ISSN 1873-4847 ; 0955-2863
    ISSN (online) 1873-4847
    ISSN 0955-2863
    DOI 10.1016/j.jnutbio.2018.08.008
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    In stock of ZB MED Bonn / Germany

    Z 5044: Show issues

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  5. Article ; Online: Calorie restriction attenuates hypertrophy-induced redox imbalance and mitochondrial ATP-sensitive K

    David, Cicera Edna Barbosa / Lucas, Aline Maria Brito / Araújo, Maria Thalyne Silva / Coelho, Beatriz Neves / Neto, Juarez Braga Soares / Portela, Bruna Raysa Campos / Varela, Anna Lídia Nunes / Kowaltowski, Alicia J / Facundo, Heberty T

    The Journal of nutritional biochemistry

    2018  Volume 62, Page(s) 87–94

    Abstract: Oxidative stress has been implicated in the pathogenesis of cardiac hypertrophy and associated heart failure. Cardiac tissue grows in response to pressure or volume overload, leading to wall thickening or chamber enlargement. If sustained, this condition ...

    Abstract Oxidative stress has been implicated in the pathogenesis of cardiac hypertrophy and associated heart failure. Cardiac tissue grows in response to pressure or volume overload, leading to wall thickening or chamber enlargement. If sustained, this condition will lead to a dysfunctional cardiac tissue and oxidative stress. Calorie restriction (CR) is a powerful intervention to improve health and delay aging. Here, we investigated whether calorie restriction in mice prevented isoproterenol-induced cardiac hypertrophy in vivo by avoiding reactive oxygen species (ROS) production and maintaining antioxidant enzymatic activity. Additionally, we investigated the involvement of mitochondrial ATP-sensitive K
    MeSH term(s) Animals ; Antioxidants/metabolism ; Caloric Restriction ; Cardiomegaly/chemically induced ; Cardiomegaly/diet therapy ; Cardiomegaly/metabolism ; Enzymes/metabolism ; Glyburide/pharmacology ; Hydrogen Peroxide/metabolism ; Isoproterenol/adverse effects ; Male ; Mice ; Oxidative Stress ; Potassium Channel Blockers/pharmacology ; Potassium Channels/metabolism ; Reactive Oxygen Species/metabolism
    Chemical Substances Antioxidants ; Enzymes ; Potassium Channel Blockers ; Potassium Channels ; Reactive Oxygen Species ; mitochondrial K(ATP) channel ; Hydrogen Peroxide (BBX060AN9V) ; Isoproterenol (L628TT009W) ; Glyburide (SX6K58TVWC)
    Language English
    Publishing date 2018-09-05
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1014929-6
    ISSN 1873-4847 ; 0955-2863
    ISSN (online) 1873-4847
    ISSN 0955-2863
    DOI 10.1016/j.jnutbio.2018.08.008
    Database MEDical Literature Analysis and Retrieval System OnLINE

    Full text online

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2838: Show issues Location:
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