title: Evaluation of the effects of fructose on oxidative stress and inflammatory parameters in rat brain.
abstract: Hereditary fructose intolerance is an autosomal recessive disorder characterized by the accumulation of fructose in tissues and biological fluids of patients. The disease results from a deficiency of aldolase B, responsible for metabolizing fructose in the liver, kidney, and small intestine. We investigated the effect of acute fructose administration on oxidative stress and neuroinflammatory parameters in the cerebral cortex of 30-day-old Wistar rats. Animals received subcutaneous injection of sodium chloride (0.9 %) (control group) or fructose solution (5 μmol/g) (fructose group). One hour later, the animals were euthanized and the cerebral cortex was isolated. Oxidative stress (levels of thiobarbituric acid-reactive substances (TBA-RS), carbonyl content, nitrate and nitrite levels, 2',7'-dihydrodichlorofluorescein (DCFH) oxidation, glutathione (GSH) levels, as well as the activities of catalase (CAT) and superoxide dismutase (SOD)) and neuroinflammatory parameters (TNF-α, IL-1β, and IL-6 levels and myeloperoxidase (MPO) activity) were investigated. Acute fructose administration increased levels of TBA-RS and carbonyl content, indicating lipid peroxidation and protein damage. Furthermore, SOD activity increased, whereas CAT activity was decreased. The levels of GSH, nitrate, and nitrite and DCFH oxidation were not altered by acute fructose administration. Finally, cytokines IL-1β, IL-6, and TNF-α levels, as well as MPO activity, were not altered. Our present data indicate that fructose provokes oxidative stress in the cerebral cortex, which induces oxidation of lipids and proteins and changes of CAT and SOD activities. It seems therefore reasonable to propose that antioxidants may serve as an adjuvant therapy to diets or to other pharmacological agents used for these patients, to avoid oxidative damage to the brain.
authors.affiliation: Laboratório de Erros Inatos do Metabolismo, Programa de Pós-Graduação em Ciências da Saúde, Unidade Acadêmica de Ciências da Saúde, Universidade do Extremo Sul Catarinense, Avenida Universitária, 1105, Bloco S, Sala 6, 88806-000, Criciúma, SC, Brazil.
authors.forename: Abigail
authors.initials: A
authors.lastname: Lopes
authors.forename: Thais Ceresér
authors.initials: TC
authors.lastname: Vilela
authors.forename: Luciane
authors.initials: L
authors.lastname: Taschetto
authors.forename: Franciele
authors.initials: F
authors.lastname: Vuolo
authors.forename: Fabricia
authors.initials: F
authors.lastname: Petronilho
authors.forename: Felipe
authors.initials: F
authors.lastname: Dal-Pizzol
authors.forename: Emilio Luiz
authors.initials: EL
authors.lastname: Streck
authors.forename: Gustavo Costa
authors.initials: GC
authors.lastname: Ferreira
authors.forename: Patrícia Fernanda
authors.initials: PF
authors.lastname: Schuck
mesh_terms: D000818:Animals; D002374:Catalase / Q000378:metabolism; D002540:Cerebral Cortex / Q000187:drug effects* / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism*; D005632:Fructose / Q000494:pharmacology*; D005978:Glutathione / Q000378:metabolism; D015227:Lipid Peroxidation / Q000187:drug effects*; D018384:Oxidative Stress / Q000187:drug effects*; D009195:Peroxidase / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D013482:Superoxide Dismutase / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism
chemical_list: D016207:Cytokines; D017392:Thiobarbituric Acid Reactive Substances; D005632:Fructose; D002374:Catalase; D009195:Peroxidase; D013482:Superoxide Dismutase; D005978:Glutathione