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Title: Oxidative stress causes hypertension and activation of nuclear factor-κB after highfructose and salt treatments.
Authors: Dornas, Waleska Claudia Amaral
Cardoso, Leonardo Máximo
Silva, Maísa
Machado, Natália Lima Santos
Chianca Júnior, Deoclécio Alves
Alzamora, Andréia Carvalho
Lima, Wanderson Geraldo de
Lagente, Vincent
Silva, Marcelo Eustáquio
Issue Date: 2017
Citation: DORNAS, W. C. et al. Oxidative stress causes hypertension and activation of nuclear factor-κB after highfructose and salt treatments. Scientific Reports, v. 7, p. 46051, 2017. Disponível em: <>. Acesso em: 29 ago. 2017.
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 fructoseinduced 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 (10mg/kg, gavage); moreover, Tempol (50mM) potentially reduced ROS production and abolished nuclear factor-kappa B (NF-κB) activation in human embryonic kidney HEK293 cells incubated with L-fructose (30mM) 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.
ISSN: 2045-2322
metadata.dc.rights.license: This work is licensed under a Creative Commons Attribution 4.0 International License. Fonte: Scientific Reports <>. Acesso em: 04 ago 2017.
Appears in Collections:DEALI - Artigos publicados em periódicos

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