Gastroprotective Effects of Zinc and Vitamin E on Some Biochemical and Histological Changes on Ethanol-Induced Mucosal Damage in Wistar Rats

Description

– Gastroprotective Effects of Zinc and Vitamin E on Some Biochemical and Histological Changes on Ethanol-Induced Mucosal Damage in Wistar Rats –

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Abstract

Antiulcerogenic effects of zinc, vitamin E and their combination on ethanol-induced ulcerogenic rats were investigated using standard methods.

The rats treated with the combination of zinc and vitamin E, followed by those treated with zinc alone and those treated with the standard drug, cimetidine had significantly (P < 0.05) higher antiulcerogenic properties as indicated by their preventive indices of 92.44 %, 89.92 %, and 73.11 % respectively compared to the rats treated with vitamin E alone (49.58 %).

Antioxidant studies revealed that vitamin E (10.01 ± 0.54 μmol/g tissue), zinc (8.77 ± 0.55μmol/g tissue) and their combination (8.52 ± 0.87 μmol/g tissue) exerted higher protective effects against lipid peroxidation, which was significantly (P < 0.05) lower than the ulcerogenic rats that were not treated and which had a value of 11.30 ±0.15 μmol/g tissue.

Superoxide dismutase (2.08 ± 0.10 U/g tissue) and glutathione peroxidase (43.17 ± 0.38 U/g tissue) activities increased significantly (P < 0.05) in the ulcerogenic groups treated with vitamin E, compared with the normal control group (1.63 ± 0.14 U/g tissue; 39.61 ± 3.18 U/g tissue).

Introduction

1.1 Background of the Study

Zinc and vitamin E are important components of biological antioxidant systems (Sahin and Kucuk, 2003). Zinc is required for growth, optimum performance and modulation of immune system, partly due to its role as a co-factor of more than two hundred enzymes (Zago and Oteiza, 2001).

An antioxidant is any agent that limits the deleterious effects of free-radical stimulated oxidant reactions. An example is vitamin E which terminates freeradical-initiated chain reactions by donating electrons to radicals (Burton and Traber, 1989).

Zinc, however, limits oxidant-induced damage in other ways through stabilization of membranes, which increases membrane resistance to oxidant damage and may downregulate radical production. (DiSilvestro, 2000).

The mechanism by which zinc exerts its antioxidant action is not well defined, but it has been suggested that it increases the synthesis of metallothionein, a cystein-rich protein, which acts as a free-radical scavenger` (Webb and Cain, 1982; Oteiza et al., 1996).

Kim et al. (1998) proposed another mode of action for zinc as an antioxidant by studying its interaction with vitamin E because; vitamin E status is impaired in zinc-deficient animals (Kim et al., 1998).

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