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Vitamin E Supplementation Modulates Endotoxin-induced Liver Damage in a Rat Model

¹Department of Microbiology, Panjab University, Chandigarh-160014, India.

²University Institute of Pharmaceutical Sciences, Panjab University, Chandigarh-160014, India.

 *Corresponding author

Dr. (Mrs.) Praveen Rishi

Department of Microbiology

Basic Medical Sciences Block

Panjab University, Chandigarh-160014.

INDIA

Telephone : (O) +91-172-2534146, 2541770;  (M): +919888895206

Fax  :  +91-172-541770 (O)

Email:   rishipraveen@yahoo.com

Abstract

Vitamin E (a-Tocopherol [a-Toc]) is the primary membrane bound, lipid-soluble, chain-breaking antioxidant that has been reported to protect against lipid peroxidation-induced tissue damage. Therefore, the present study was designed to investigate the protection afforded by a-Tocopherol (vitamin E), if any, on LPS-induced liver injury in Wistar rats and to study the underlying mechanism of protection. Bacterial endotoxin (10 mg/Kg body weight-prestandardized dose) was injected intraperitoneally and animals were sacrificed 8 h post-challenge. Vitamin E (35 mg/Kg body weight) was administered orally for 15 days prior to endotoxin challenge. Challenge with LPS resulted in a significant increase in the activities of serum transaminases and alkaline phosphatase along with histological alterations in the liver. These responses were associated with elevated levels of malondialdehyde (MDA) and reduced levels of glutathione, superoxide dismutase and catalase along with increased levels of tumor necrosis factor alpha (TNF-a) in the liver homogenates. However, vitamin E supplementation attenuated the oxidative stress by reducing the levels of MDA, restoring the levels of glutathione, superoxide dismutase and catalase and decreasing the levels of TNF-a. Decreased TNF-a levels after vitamin E supplementation might have resulted into the modulation of above mentioned biochemical changes resulting into amelioration of hepatic architecture. Vitamin E, therefore, seems to have a promising role for clinical manifestations due to oxidative stress.

Keywords:  Endotoxin; Liver; Oxidative stress; a-Tocopherol; Tumor necrosis factor alpha.

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