Choline and Cystine Deficient Diets in Animal Models with Hepatocellular Injury: Evaluation of Oxidative Stress and Expression of RAGE, TNF-[alpha], and IL-1[beta]

• Published in: Oxidative medicine and cellular longevity Vol. 2015
• Main Authors: Santos, Juliana Celia F, Orlando R. P. de Araújo, Valentim, Iara B, Kivia Queiroz de Andrade, Moura, Fabiana Andrea, Smaniotto, Salete, Marques dos Santos, John, Gasparotto, Juciano, Gelain, Daniel P, Goulart, Marilia O F
• Format: Journal Article
• Language: English
• Published: New York Hindawi Limited 01-01-2015
• Subjects: Antioxidants; Cytokines; Defense; Diabetes; Diet; Disease; Inflammation; Laboratory animals; Liver; Metabolism; Nutrition research; Oxidative stress; Proteins; Rodents; Studies
• ISSN: 1942-0900; 1942-0994
• DOI: 10.1155/2015/121925

This study aims to evaluate the effects of diets deficient in choline and/or cystine on hepatocellular injury in animal models (young male Wistar rats, aged 21 days), by monitoring some of the oxidative stress biomarkers and the expression of RAGE, TNF-α, and IL-1β. The animals were divided into 6 groups (n=10) and submitted to different diets over 30 days: AIN-93 diet (standard, St), AIN-93 choline deficient (CD) diet and AIN-93 choline and cystine deficient (CCD) diet, in the pellet (pl) and powder (pw) diet forms. Independently of the diet form, AIN-93 diet already led to hepatic steatosis and CD/CCD diets provoked hepatic damage. The increase of lipid peroxidation, represented by the evaluation of thiobarbituric acid reactive species, associated with the decrease of levels of antioxidant enzymes, were the parameters with higher significance toward redox profile in this model of hepatic injury. Regarding inflammation, in relation to TNF-α, higher levels were evidenced in [subscript]CD(pl)[/subscript] , while, for IL-1β, no significant alteration was detected. RAGE expression was practically the same in all groups, with exception of [subscript]CCD(pw)[/subscript] versus [subscript]CCD(pl)[/subscript] . These results together confirm that AIN-93 causes hepatic steatosis and choline and/or cysteine deficiencies produce important hepatic injury associated with oxidative stress and inflammatory profiles.