Vitamin C and Vitamin E in Prevention of Nonalcoholic Fatty Liver Disease (NAFLD) in Choline Deficient Diet Fed Rats


Autoria(s): Oliveira, Claudia PMS; Gayotto, Luiz ; Tatai, Caroline ; Nina, Bianca ; Lima, Emerson S; Abdalla, Dulcinéia SP; Lopasso, Fabio P; Laurindo, Francisco RM; Carrilho, Flair 
Contribuinte(s)

UNIVERSIDADE DE SÃO PAULO

Data(s)

26/08/2013

26/08/2013

2003

Resumo

Abstract Aim Oxidative stress has been implicated in the pathogenesis of Nonalcoholic Fatty Liver Disease (NAFLD). Vitamin C and vitamin E are known to react with reactive oxygen species (ROS) blocking the propagation of radical reactions in a wide range of oxidative stress situations. The potential therapeutic efficacy of antioxidants in NAFLD is unknown. The aim of this study was to evaluate the role of antioxidant drugs (vitamin C or vitamin E) in its prevention. Methods Fatty liver disease was induced in Wistar rats by choline-deficient diet for four weeks. The rats were randomly assigned to receive vitamin E (n = 6) – (200 mg/day), vitamin C (n = 6) (30 mg/Kg/day) or vehicle orally. Results In the vehicle and vitamin E-treated rats, there were moderate macro and microvesicular fatty changes in periportal area without inflammatory infiltrate or fibrosis. Scharlach stain that used for a more precise identification of fatty change was strong positive. With vitamin C, there was marked decrease in histological alterations. Essentially, there was no liver steatosis, only hepatocellular ballooning. Scharlach stain was negative. The lucigenin-enhanced luminescence was reduced with vitamin C (1080 ± 330 cpm/mg/minx103) as compared to those Vitamin E and control (2247 ± 790; 2020 ± 407 cpm/mg/minx103, respectively) (p < 0.05). Serum levels of aminotransferases were unaltered by vitamin C or vitamin E. Conclusions 1) Vitamin C reduced oxidative stress and markedly inhibited the development of experimental liver steatosis induced by choline-deficient diet ; 2)Vitamin E neither prevented the development of fatty liver nor reduced the oxidative stress in this model.

Identificador

Nutrition Journal, 2(1), Oct 2003

1475-2891

http://www.producao.usp.br/handle/BDPI/32971

10.1186/1475-2891-2-9

http://www.nutritionj.com/content/2/1/9

Idioma(s)

eng

Relação

Nutrition Journal

Direitos

openAccess

Oliveira et al; licensee BioMed Central Ltd. This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose, provided this notice is preserved along with the article's original URL. -

Tipo

article

original article