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  1. Article ; Online: Animal models for the study of arterial hypertension.

    Dornas, Waleska C / Silva, Marcelo E

    Journal of biosciences

    2011  Volume 36, Issue 4, Page(s) 731–737

    Abstract: Hypertension is one of the leading causes of disability or death due to stroke, heart attack and kidney failure. Because the etiology of essential hypertension is not known and may be multifactorial, the use of experimental animal models has provided ... ...

    Abstract Hypertension is one of the leading causes of disability or death due to stroke, heart attack and kidney failure. Because the etiology of essential hypertension is not known and may be multifactorial, the use of experimental animal models has provided valuable information regarding many aspects of the disease, which include etiology, pathophysiology, complications and treatment. The models of hypertension are various, and in this review, we provide a brief overview of the most widely used animal models, their features and their importance.
    MeSH term(s) Animals ; Denervation/adverse effects ; Diet/adverse effects ; Disease Models, Animal ; Humans ; Hypertension/etiology ; Hypertension/genetics ; Hypertension/physiopathology ; Hypertension, Renal/etiology ; Hypertension, Renal/genetics ; Hypertension, Renal/physiopathology ; Models, Animal ; NG-Nitroarginine Methyl Ester/pharmacology ; Nitric Oxide/antagonists & inhibitors ; Nitric Oxide/metabolism ; Nitric Oxide Synthase/antagonists & inhibitors ; Nitric Oxide Synthase/metabolism ; Pressoreceptors/surgery ; Rats ; Rats, Inbred Dahl ; Rats, Inbred SHR ; Rats, Transgenic
    Chemical Substances Nitric Oxide (31C4KY9ESH) ; Nitric Oxide Synthase (EC 1.14.13.39) ; NG-Nitroarginine Methyl Ester (V55S2QJN2X)
    Language English
    Publishing date 2011-08-21
    Publishing country India
    Document type Journal Article ; Review
    ZDB-ID 756157-x
    ISSN 0973-7138 ; 0250-5991
    ISSN (online) 0973-7138
    ISSN 0250-5991
    DOI 10.1007/s12038-011-9097-y
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1907: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
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  2. Article ; Online: Health implications of high-fructose intake and current research.

    Dornas, Waleska C / de Lima, Wanderson G / Pedrosa, Maria L / Silva, Marcelo E

    Advances in nutrition (Bethesda, Md.)

    2015  Volume 6, Issue 6, Page(s) 729–737

    Abstract: Although fructose consumption has dramatically increased and is suspected to be causally linked to metabolic abnormalities, the mechanisms involved are still only partially understood. We discuss the available data and investigate the effects of dietary ... ...

    Abstract Although fructose consumption has dramatically increased and is suspected to be causally linked to metabolic abnormalities, the mechanisms involved are still only partially understood. We discuss the available data and investigate the effects of dietary fructose on risk factors associated with metabolic disorders. The evidence suggests that fructose may be a predisposing cause in the development of insulin resistance in association with the induction of hypertriglyceridemia. Experiments in animals have shown this relation when they are fed diets very high in fructose or sucrose, and human studies also show this relation, although with conflicting results due to the heterogeneity of the studies. The link between increased fructose consumption and increases in uric acid also has been confirmed as a potential risk factor for metabolic syndrome, and insulin resistance/hyperinsulinemia may be causally related to the development of hypertension. Collectively, these results suggest a link between high fructose intake and insulin resistance, although future studies must be of reasonable duration, use defined populations, and improve comparisons regarding the effects of relevant doses of nutrients on specific endpoints to fully understand the effect of fructose intake in the absence of potential confounding factors.
    MeSH term(s) Animals ; Diet ; Dietary Sucrose/administration & dosage ; Fructose/administration & dosage ; Fructose/adverse effects ; Fructose/metabolism ; Humans ; Hypertension/etiology ; Hypertriglyceridemia/etiology ; Insulin/blood ; Insulin Resistance ; Lipid Metabolism ; Metabolic Diseases/etiology ; Mice ; Obesity/etiology ; Rats ; Risk Factors ; Uric Acid/blood ; Weight Gain
    Chemical Substances Dietary Sucrose ; Insulin ; Uric Acid (268B43MJ25) ; Fructose (30237-26-4)
    Language English
    Publishing date 2015-11-13
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 2583634-1
    ISSN 2156-5376 ; 2156-5376
    ISSN (online) 2156-5376
    ISSN 2156-5376
    DOI 10.3945/an.114.008144
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Efficacy of the superoxide dismutase mimetic tempol in animal hypertension models: a meta-analysis.

    Dornas, Waleska C / Silva, Maísa / Tavares, Ricardo / de Lima, Wanderson G / dos Santos, Rinaldo C / Pedrosa, Maria L / Silva, Marcelo E

    Journal of hypertension

    2015  Volume 33, Issue 1, Page(s) 14–23

    Abstract: Objective: Considering the growing body of evidence that indicates the contribution of superoxide anions (O2) and other reactive oxygen species (ROS) to the development of hypertension, we assessed whether animal models of hypertension have a benefic ... ...

    Abstract Objective: Considering the growing body of evidence that indicates the contribution of superoxide anions (O2) and other reactive oxygen species (ROS) to the development of hypertension, we assessed whether animal models of hypertension have a benefic effect with tempol, a superoxide dismutase mimetic, to help augment the design of future studies.
    Methods: Studies published between July 1998 and December 2012 on blood pressure (BP) in different hypertensive models were obtained after an electronic and manual search of PubMed. In-depth analyses of the methodological quality of the studies and the mean arterial pressure (MAP) changes after treatment with tempol were performed, as well as the subgroup analyses on the route of tempol delivery.
    Results: Out of the 144 identified studies, 28 were included after screening. The data showed that tempol reduced MAP by computing the standardized mean difference with the value of 4.622 (95% confidence interval 3.24-5.99). The quality of studies included in the meta-analysis was category II; however, omission of details in the trials might have biased the results. There was substantial heterogeneity in the results with an I of 94.45%, which persisted after stratifying for the route of tempol delivery.
    Conclusion: In conclusion, this analysis shows that antioxidant treatment with tempol can reduce BP, suggesting that ROS plays a role in the pathogenesis of increased BP in the hypertension models used in the current research practice.
    MeSH term(s) Animals ; Antioxidants/therapeutic use ; Biomimetic Materials/pharmacology ; Biomimetic Materials/therapeutic use ; Blood Pressure/drug effects ; Blood Pressure/physiology ; Cyclic N-Oxides/pharmacology ; Cyclic N-Oxides/therapeutic use ; Disease Models, Animal ; Hypertension/drug therapy ; Hypertension/metabolism ; Rats ; Spin Labels ; Superoxide Dismutase/pharmacology ; Superoxide Dismutase/therapeutic use ; Superoxides/metabolism
    Chemical Substances Antioxidants ; Cyclic N-Oxides ; Spin Labels ; Superoxides (11062-77-4) ; Superoxide Dismutase (EC 1.15.1.1) ; tempol (U78ZX2F65X)
    Language English
    Publishing date 2015-01
    Publishing country England
    Document type Journal Article ; Meta-Analysis ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 605532-1
    ISSN 1473-5598 ; 0263-6352 ; 0952-1178
    ISSN (online) 1473-5598
    ISSN 0263-6352 ; 0952-1178
    DOI 10.1097/HJH.0000000000000422
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1885: Show issues Location:
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    Zs.MO 614: Show issues

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  4. Article ; Online: Oxidative stress causes hypertension and activation of nuclear factor-κB after high-fructose and salt treatments.

    Dornas, Waleska C / Cardoso, Leonardo M / Silva, Maísa / Machado, Natália L S / Chianca, Deoclécio A / Alzamora, Andréia C / Lima, Wanderson G / Lagente, Vincent / Silva, Marcelo E

    Scientific reports

    2017  Volume 7, Page(s) 46051

    Abstract: There is evidence that diets rich in salt or simple sugars as fructose are associated with abnormalities in blood pressure regulation. However, the mechanisms underlying pathogenesis of salt- and fructose-induced kidney damage and/or consequent ... ...

    Abstract There is evidence that diets rich in salt or simple sugars as fructose are associated with abnormalities in blood pressure regulation. However, the mechanisms underlying pathogenesis of salt- and fructose-induced kidney damage and/or consequent hypertension yet remain largely unexplored. Here, we tested the role of oxidative state as an essential factor along with high salt and fructose treatment in causing hypertension. Fischer male rats were supplemented with a high-fructose diet (20% in water) for 20 weeks and maintained on high-salt diet (8%) associate in the last 10 weeks. Fructose-fed rats exhibited a salt-dependent hypertension accompanied by decrease in renal superoxide dismutase activity, which is the first footprint of antioxidant inactivation by reactive oxygen species (ROS). Metabolic changes and the hypertensive effect of the combined fructose-salt diet (20 weeks) were markedly reversed by a superoxide scavenger, Tempol (10 mg/kg, gavage); moreover, Tempol (50 mM) potentially reduced ROS production and abolished nuclear factor-kappa B (NF-κB) activation in human embryonic kidney HEK293 cells incubated with L-fructose (30 mM) and NaCl (500 mosmol/kg added). Taken together, our data suggested a possible role of oxygen radicals and ROS-induced activation of NF-κB in the fructose- and salt-induced hypertension associated with the progression of the renal disease.
    MeSH term(s) Antioxidants/metabolism ; Blood Pressure ; Body Weight ; Cyclic N-Oxides/pharmacology ; Diet ; Drinking Behavior ; Feeding Behavior ; Fructose/adverse effects ; Gene Expression Regulation/drug effects ; Glucose Tolerance Test ; HEK293 Cells ; Humans ; Hypertension/blood ; Hypertension/metabolism ; Hypertension/pathology ; Hypertension/physiopathology ; Kidney/drug effects ; Kidney/enzymology ; Kidney/pathology ; Lymphocytes/drug effects ; Lymphocytes/metabolism ; Monocytes/drug effects ; Monocytes/metabolism ; NF-kappa B/metabolism ; Oxidative Stress/drug effects ; Reactive Oxygen Species/metabolism ; Sodium Chloride/adverse effects ; Spin Labels ; Superoxide Dismutase/metabolism
    Chemical Substances Antioxidants ; Cyclic N-Oxides ; NF-kappa B ; Reactive Oxygen Species ; Spin Labels ; Fructose (30237-26-4) ; Sodium Chloride (451W47IQ8X) ; Superoxide Dismutase (EC 1.15.1.1) ; tempol (U78ZX2F65X)
    Language English
    Publishing date 2017-04-11
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/srep46051
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Experimental atherosclerosis in rabbits.

    Dornas, Waleska C / Oliveira, Tânia T de / Augusto, Luis E Franklin / Nagem, Tanus J

    Arquivos brasileiros de cardiologia

    2010  Volume 95, Issue 2, Page(s) 272–278

    Abstract: Many researches have been conducted in experimental models in order to study the development of atherosclerosis from hyperlipidemia-inducing diets. Since rabbits are very sensitive to cholesterol-rich diets and accumulate large amounts of cholesterol in ... ...

    Abstract Many researches have been conducted in experimental models in order to study the development of atherosclerosis from hyperlipidemia-inducing diets. Since rabbits are very sensitive to cholesterol-rich diets and accumulate large amounts of cholesterol in their plasma, their use as experimental models to evaluate the development of atherosclerosis is highly relevant and brings information on factors that contribute to the progression and regression of this condition that can be applied to humans. As such, this review includes studies on the atherogenic function of cholesterol based on rabbits as the experimental model, since they have become the most largely used experimental model of atherosclerosis.
    MeSH term(s) Animals ; Atherosclerosis/etiology ; Atherosclerosis/pathology ; Cholesterol/blood ; Cholesterol, Dietary/administration & dosage ; Cholesterol, Dietary/adverse effects ; Coronary Vessels/pathology ; Diet ; Diet, Atherogenic ; Disease Models, Animal ; Endothelium, Vascular/pathology ; Endothelium, Vascular/physiopathology ; Hypercholesterolemia/complications ; Hypercholesterolemia/metabolism ; Rabbits
    Chemical Substances Cholesterol, Dietary ; Cholesterol (97C5T2UQ7J)
    Language Portuguese
    Publishing date 2010-09-24
    Publishing country Brazil
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 730261-7
    ISSN 1678-4170 ; 0066-782X
    ISSN (online) 1678-4170
    ISSN 0066-782X
    DOI 10.1590/s0066-782x2010001200020
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 548: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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  6. Article ; Online: Iron toxicity mediated by oxidative stress enhances tissue damage in an animal model of diabetes.

    Sampaio, Ana Flávia S / Silva, Maisa / Dornas, Waleska C / Costa, Daniela C / Silva, Marcelo E / Dos Santos, Rinaldo C / de Lima, Wanderson G / Pedrosa, Maria Lúcia

    Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine

    2014  Volume 27, Issue 2, Page(s) 349–361

    Abstract: Although iron is a first-line pro-oxidant that modulates clinical manifestations of various systemic diseases, including diabetes, the individual tissue damage generated by active oxidant insults has not been demonstrated in current animal models of ... ...

    Abstract Although iron is a first-line pro-oxidant that modulates clinical manifestations of various systemic diseases, including diabetes, the individual tissue damage generated by active oxidant insults has not been demonstrated in current animal models of diabetes. We tested the hypothesis that oxidative stress is involved in the severity of the tissues injury when iron supplementation is administered in a model of type 1 diabetes. Streptozotocin (Stz)-induced diabetic and non-diabetic Fischer rats were maintained with or without a treatment consisting of iron dextran ip at 0.1 mL day(-1) doses administered for 4 days at intervals of 5 days. After 3 weeks, an extensive increase (p < 0.001) in the production of reactive oxygen species (ROS) in neutrophils of the diabetic animals on iron overload was observed. Histological analysis revealed that this treatment also resulted in higher (p < 0.05) tissue iron deposits, a higher (p < 0.001) number of inflammatory cells in the pancreas, and apparent cardiac fibrosis, as shown by an increase (p < 0.05) in type III collagen levels, which result in dysfunctional myocardial. Carbonyl protein modification, a marker of oxidative stress, was consistently higher (p < 0.01) in the tissues of the iron-treated rats with diabetes. Moreover, a significant positive correlation was found between ROS production and iron pancreas stores (r = 0.42, p < 0.04), iron heart stores (r = 0.54, p < 0.04), and change of the carbonyl protein content in pancreas (r = 0.49, p < 0.009), and heart (r = 0.48, p < 0.02). A negative correlation was still found between ROS production and total glutathione content in pancreas (r = -0.50, p < 0.03) and heart (r = -0.45, p < 0.04). In conclusion, our results suggest that amplified toxicity in pancreatic and cardiac tissues in rats with diabetes on iron overload might be attributed to increased oxidative stress.
    MeSH term(s) Animals ; Diabetes Mellitus, Experimental/chemically induced ; Diabetes Mellitus, Experimental/complications ; Diabetes Mellitus, Experimental/metabolism ; Diabetes Mellitus, Experimental/pathology ; Diabetes Mellitus, Type 1/chemically induced ; Diabetes Mellitus, Type 1/metabolism ; Diabetes Mellitus, Type 1/pathology ; Disease Models, Animal ; Iron Overload/chemically induced ; Iron Overload/complications ; Iron Overload/metabolism ; Iron-Dextran Complex/administration & dosage ; Iron-Dextran Complex/pharmacokinetics ; Iron-Dextran Complex/toxicity ; Male ; Oxidative Stress/drug effects ; Rats ; Rats, Inbred F344 ; Reactive Oxygen Species/metabolism ; Streptozocin ; Tissue Distribution
    Chemical Substances Reactive Oxygen Species ; Streptozocin (5W494URQ81) ; Iron-Dextran Complex (9004-66-4)
    Language English
    Publishing date 2014-04
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1112688-7
    ISSN 1572-8773 ; 0966-0844
    ISSN (online) 1572-8773
    ISSN 0966-0844
    DOI 10.1007/s10534-014-9717-8
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 2515: Show issues Location:
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