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

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/minx10 3 ) as compared to those Vitamin E and control (2247 ± 790; 2020 ± 407 cpm/mg/minx10 3 , 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.

Effect of lycopene on oxidative stress induced duringd-galactosamine/lipopolysaccharide-sensitized liver injury in rats

“…The tissue concentration of these antioxidants is a good indicator of oxidative stress. The clear inverse association between the oxidative stress during liver injury and levels of these antioxidants were well documented and the decreased values of these vitamins in this study is clearly in accordance with previous findings (Krishnamoorthi & Sangeetha, 2008;Oliveira et al, 2003;Saraswathy et al, 2010). Lycopene pretreatment restores the altered levels of these vitamins during D-GalN/LPS toxicity through its antioxidant defense.…”

<a name="home"></a>Liver mitochondrial dysfunction and oxidative stress in the pathogenesis of experimental nonalcoholic fatty liver disease

“…Drug-induced fatty liver has increased lipid peroxidation (17) and ob/ob mice have an increased ROS production (11). Our group has demonstrated in previous studies that the presence of steatosis correlates with an increase in superoxide anion hydroperoxide generation in animals fed a choline-deficient diet (18) and the use of vitamin C reduces liver steatosis and peroxidation (19). In the present study, lipid peroxidation was also increased and GSH was decreased in the CD group while the oxidative stress of animals fed a high-fat diet enriched with PUFAs-ω-3 was similar to that observed in controls.…”

Progression of Lipid Peroxidation Measured as Thiobarbituric Acid Reactive Substances, Damage to DNA and Histopathological Changes in the Liver of Rats Subjected to a Methionine–Choline‐Deficient Diet

“…A study has shown that vitamin C reduced oxidative stress and markedly inhibited the development of experimental liver steatosis induced by a choline-deficient diet but vitamin E neither prevented the development of fatty liver nor reduced the oxidative stress in this model [26].…”