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High‐fat diet and hydrochlorothiazide increase oxidative stress in brain of rats
Author(s) -
Ribeiro Marinei Cristina Pereira,
Barbosa Nilda Berenice de Vargas,
de Almeida Tielle Moraes,
Parcianello Lutiane Mozzaquatro,
Perottoni Juliano,
de Ávila Daiana Silva,
Rocha João Batista Teixeira
Publication year - 2009
Publication title -
cell biochemistry and function
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.933
H-Index - 61
eISSN - 1099-0844
pISSN - 0263-6484
DOI - 10.1002/cbf.1599
Subject(s) - hydrochlorothiazide , endocrinology , oxidative stress , medicine , lipid peroxidation , chemistry , npsh , vitamin e , antioxidant , pharmacology , biochemistry , blood pressure , glutathione , enzyme
This study evaluated the effect of possible synergic interaction between high fat diet (HF) and hydrochlorothiazide (HCTZ) on biochemical parameters of oxidative stress in brain. Rats were fed for 16 weeks with a control diet or with an HF, both supplemented with different doses of HCTZ (0.4, 1.0, and 4.0 g kg −1 of diet). HF associated with HCTZ caused a significant increase in lipid peroxidation and blood glucose levels. In addition, HF ingestion was associated with an increase in cerebral lipid peroxidation, vitamin C and non‐protein thiol groups (NPSH) levels. There was an increase in vitamin C as well as NPSH levels in HCTZ (1.0 and 4.0 g kg −1 of diet) and HF plus HCTZ groups. Na + –K + ‐ATPase activity of HCTZ (4.0 g kg −1 of diet) and HCTZ plus HF‐fed animals was significantly inhibited. Our data indicate that chronic intake of a high dose of HCTZ (4 g kg −1 of diet) or HF change biochemical indexes of oxidative stress in rat brain. Furthermore, high‐fat diets consumption and HCTZ treatment have interactive effects on brain, showing that a long‐term intake of high‐fat diets can aggravate the toxicity of HCTZ. Copyright © 2009 John Wiley & Sons, Ltd.