Diphenyl diselenide supplementation reduces biochemical alterations associated with oxidative stress in rats fed with fructose and hydrochlorothiazide

作者:Pereira Ribeiro Marinei Cristina; Avila Daiana Silva; Pires Schiar Viviane Patricia; dos Santos Danubia Bonfanti; Meinerz Daiane F; Frescura Duarte Marta Medeiros; Monteiro Roger; Puntel Robson; de Bem Andreza Fabro; Hassan Waseem; de Vargas Barbosa Nilda Berenice; Teixeira Rocha Joao Batista
来源:Chemico-Biological Interactions, 2013, 204(3): 191-199.
DOI:10.1016/j.cbi.2013.05.008

摘要

The study evaluated whether a diet containing diphenyl diselenide (PhSe)(2), a synthetic antioxidant, could reduce the biochemical alterations induced by chronic consumption of highly enriched fructose diet and/or hydrochlorothiazide (HCTZ). Rats were fed a control diet (CT) or a high fructose diet (HFD), supplemented with or not HCTZ (4.0 g/kg) and/or (PhSe)(2) (3 ppm) for 18 weeks. HFD intake increased significantly plasma glucose, fructosamine, triglycerides and cholesterol levels. (PhSe)(2) supplementation significantly reduced triglycerides and cholesterol but could not restore them to control levels. The combination of HFD and HCTZ significantly altered plasma glucose, fructosamine, triglycerides and cholesterol levels which were not restore by (PhSe)(2) supplementation. Lipid peroxidation, protein carbonyl formation, vitamin C level and catalase activity decreased after HFD, HCTZ or HFD plus HCTZ ingestion. Remarkably (PhSe)(2) supplementation restored the oxidative stress parameters. HCTZ decreased renal superoxide dismutase (SOD) activity, which was restored to control levels by (PhSe)(2). Furthermore, the association of HFD and HCTZ decreased plasma potassium levels and aggravated HCTZ-induced hypomagnesemia and hypertriglyceridemia. Here we provided evidence of the involvement of oxidative stress and metabolic disorders in a rat model of HFD associated or not with HTCZ. (PhSe)(2) supplementation reduced the oxidative stress and this compound should be considered for the treatment of biochemical disturbances and oxidative stress in other animal models of metabolic disorders.

  • 出版日期2013-8-25