Effects of chronic ethanol and vitamin C administration on production of tumor necrosis factor-a and interleukin-6 in rats

1Mervat A.El-Taukhy, 2Suzan M. Salama, 3Seham A. Abou-Shousha 4Saad S. Ismail and 1Marium Saleh

Departments of 1applied medical chemistry, 2Biochemistry, 3Immunology and 4Pharmacology, Medical Research Institute, Alexandria University, Alexandria, Egypt.

Chronic alcoholism complicated by alcoholic liver disease (ALD) is characterized by activation of inflammatory responses. Alcohol intake increases gut permeability allowing substances such as lipopolysaccharides (LPS) which are strong inducers of proinflammatory cytokines such as tumor necrosis factor-alpha (TNF-a) and interleukin-6 (IL-6) to enter the circulation. Vitamin C is an antioxidant with many cellular activities seemed to protect cells against alcohol-induced peroxidation. In present study, serum levels of TNF-a and IL-6 were measured by ELISA method in four groups of albino rats, each group consists of 10 rats. Group (I) was untreated group (control), group (II) was treated with ethanol, group (III) was treated with ascorbic acid and group (IV) was treated with ethanol + ascorbic acid. Results revealed that both TNF- a and IL-6 serum levels were very highly significantly increased in group (II) and (IV) than control group (1) (P < 0.001). Group (III) showed significantly (P < 0.001) decreased TNF-a serum level than group (II) and (IV) while it showed significantly (P < 0.001) increased IL-6 serum level than control group (I) and also significantly decreased IL-6 serum level than group (IV). Serum IL-6 level was significantly (P < 0.01) decreased in group (III) than (II). These results indicate that serum levels of the proinflammatory cytokines TNF-a and IL-6 may serve as predictive biomarkers for progression of ALD. In addition, using TNF-a neutralizing agent (or its antagonist)/or IL-6 as an anti-apoptotic factor could be useful as a treatment strategy of ALD.