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Molecular mechanisms related to the hepatoprotective effects of antioxidant-rich extra virgin olive oil supplementation in rats subjected to short-term iron administration.
Barrera, Cynthia; Valenzuela, Rodrigo; Rincón, Miguel Ángel; Espinosa, Alejandra; Echeverria, Francisca; Romero, Nalda; Gonzalez-Mañan, Daniel; Videla, Luis A.
Afiliação
  • Barrera C; Department of Nutrition, Faculty of Medicine, University of Chile, Santiago, Chile.
  • Valenzuela R; Department of Nutrition, Faculty of Medicine, University of Chile, Santiago, Chile; Lipid Center, Institute of Nutrition and Food Technology, University of Chile, Santiago, Chile. Electronic address: rvalenzuelab@med.uchile.cl.
  • Rincón MÁ; Lipid Center, Institute of Nutrition and Food Technology, University of Chile, Santiago, Chile.
  • Espinosa A; Department of Medical Technology, Faculty of Medicine, University of Chile, Santiago, Chile.
  • Echeverria F; Department of Nutrition, Faculty of Medicine, University of Chile, Santiago, Chile.
  • Romero N; Department of Food Science and Chemical Technology, Faculty of Chemical Sciences and Pharmacy, University of Chile, Santiago, Chile.
  • Gonzalez-Mañan D; Núcleo de Química y Bioquímica, Facultad de Ciencias, Universidad Mayor, Chile.
  • Videla LA; Molecular and Clinical Pharmacology Program, Institute of Biomedical Sciences, Faculty of Medicine, University of Chile, Santiago-7, Chile.
Free Radic Biol Med ; 126: 313-321, 2018 10.
Article em En | MEDLINE | ID: mdl-30153476
Enhanced iron levels in liver are associated with oxidative stress development and damage with increased fat accumulation. The aim of this work was to assess the hypothesis that antioxidant-rich extra virgin olive oil (AR-EVOO) counteracts iron-rich diet (IRD)-induced oxidative stress hindering hepatic steatosis. Male Wistar rats were fed and IRD (200 mg iron/kg diet) versus a control diet (CD; 50 mg iron/kg diet) with alternate AR-EVOO supplementation (100 mg/day) for 21 days. IRD induced liver steatosis and oxidative stress (higher levels of protein oxidation and lipid peroxidation with glutathione depletion), mitochondrial dysfunction (decreased citrate synthase and complex I and II activities) and loss of polyunsaturated fatty acids (PUFAs), with a drastic enhancement in the sterol regulatory element-binding protein-1c (SREBP-1c)/peroxisome proliferator-activated receptor-α (PPAR-α) ratio upregulating the expression of lipogenic enzymes (acetyl-CoA carboxylase, fatty acid (FA) synthase and stearoyl desaturase 2) and downregulating those involved in FA oxidation (carnitine palmitoyl transferase and acyl-CoA oxidase) over values in the CD group. IRD also upregulated nuclear factor erythroid 2-related factor 2 (Nrf2) and its target genes. AR-EVOO supplementation alone did not modify the studied parameters, however, IRD combined with AR-EVOO administration returned IRD-induced changes to baseline levels of the CD group. It is concluded that IRD-induced non-alcoholic fatty liver disease (NAFLD) is prevented by AR-EVOO supplementation, which might be related to the protective effects of its components such as hydroxytyrosol, oleic acid, tocopherols and/or PUFAs, thus representing a suitable anti-steatotic strategy to avoid progression into more severe stages of the disease, underlying NAFLD associated with iron overloading pathologies or obesity.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Suplementos Nutricionais / Hepatopatia Gordurosa não Alcoólica / Azeite de Oliva / Antioxidantes Limite: Animals / Humans Idioma: En Revista: Free Radic Biol Med Assunto da revista: BIOQUIMICA / MEDICINA Ano de publicação: 2018 Tipo de documento: Article País de afiliação: Chile País de publicação: Estados Unidos

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Suplementos Nutricionais / Hepatopatia Gordurosa não Alcoólica / Azeite de Oliva / Antioxidantes Limite: Animals / Humans Idioma: En Revista: Free Radic Biol Med Assunto da revista: BIOQUIMICA / MEDICINA Ano de publicação: 2018 Tipo de documento: Article País de afiliação: Chile País de publicação: Estados Unidos