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

Claudia PMS Oliveira1*, Luiz Carlos da Costa Gayotto2, Caroline Tatai1, Bianca Ishimoto Della Nina1, Emerson S Lima4, Dulcinéia SP Abdalla4, Fabio P Lopasso1, Francisco RM Laurindo3 and Flair José Carrilho1

Author affiliations

1 Department of Gastroenterology of Medical School of University of São Paulo (USP), São Paulo, Brazil

2 Department of Pathology (LIM14) of Medical School of University of São Paulo (USP), São Paulo, Brazil

3 Departament of Heart Institute of Medical School of University of São Paulo (USP), São Paulo, Brazil

4 Department of Clinical and Toxicological Analyses of School of Pharmaceutical Sciences of University of São Paulo (USP), São Paulo, Brazil

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Citation and License

Nutrition Journal 2003, 2:9  doi:10.1186/1475-2891-2-9

Published: 7 October 2003



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.


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.


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.


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.

vitamin C; vitamin E; nonalcoholic fatty liver disease; oxidative stress