Abstract:
Damage to gastric mucosa
caused by restraint stress has been attributed to impaired blood flow
that resulted in ischemia followed by reperfusion, a process that generates
free radicals. Therefore oxygen radicals may mediate the lesions produced
in restraint stress. To test this hypothesis, we studied the effect
of free radical scavengers on restraint-induced lesions in rats. Forty
rats were divided in to four groups of 10 rats. Two control groups was
fed with a normal rat diet and two treatment groups fed with a vitamin
E deficient diet with either tocopherol or tocotrienol, which serves
as free radical scavengers. The two forms of vitamin E were administered
orally at 60mg/kg body weight for 28 days. After 28 days, rats from
one control group and the two treated groups were subjected to restraint
stress 2 hours daily for 4 consecutive days. The rats were killed after
the fourth exposure, their stomach isolated and examined for lesions,
and gastric malondialdehyde (MOA) content and the gastric reduced glutathione
level were measured as an index to reflect the scavenging abilities
of tocopherol and tocotrienol. Both the regimes significantly attenuated
the total lesion area in the stomach compared to the control. The MOA
content was also significantly lower in the rats given tocopherol and
tocotrienol supplementation compared to the control and the reduced
glutathione levels were preserved in rats supplemented with both tocopherol
and tocotrienol. We conclude that it is indeed probable that oxygen
radical is involved in the pathogenesis of restraint stress-induced
lesions thus supplementation with antioxidant such as vitamin E may
be able to reduce or inhibit the formation of these lesions.
M.F. Nur Azlina , M.I. Nafeeza and B.A.K. Khalid , 2005. Effect of Tocotrienol on Lipid Peroxidation in Experimental Gastritis Induced by Restraint Stress. Pakistan Journal of Nutrition, 4: 69-72.
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