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Abstract
from the obtained results in the present study it could be concluded that:
Long-term treatment of rats with aluminium chloride might inhibit glycolysis (as indicating by the increase of the plasma glucose levels) and might impair liver and kidney functions by increase the plasma the plasma levels of ALT, AST and uric acid.
It also increased total lipids, triglycerides and total thiols in plasma, but decreased plasma levels of cholesterol and alkaline phosphatase.
Aluminium was found to induce oxidative damage damage in treated rats where it increased the lipid peroxative damage in treated rats where it increased the lipid peroxides levels as thiobarbaturic acid reactive substance in plasma, erythrocytes lysate kidney and liver tissues.
It also elevated the levels of nitric oxides as nitrite in plasma, kidney and brain tissues.
At the same time, aluminium was shown to inhibit the activity of antioxidant enzymes; SOD in plasma, liver and brain tissues and catalase in liver, kidney and brain tissues.
But the activity of glutathione s-transferase toward CDNB as a substrate showed as significant increase in liver tissues due to the chronicity of aluminium.
Also aluminium was shown to exhaust glutathione content in erythrocytes lysate and tissue and vitamin E content in plasma and brain tissues.
Tannic acid (a polyphenoic compound)was reported earlier as antioxidant prevented hydroxyI radical formation in fenton reaction due iron chelation.
It was proposed in the present study as protective agent againt long-term treatment of rats with aluminium chloride, showing the following effects:
It inhibited the toxic action of aluminium chloride on glucose metabolism;
It impaired the toxic action of aluminium chloride on kidney and liver functions;
It preserver total lipid levels in plasma, but failed to prevent the elevation of triglycerides levels.
Long-term treatment of rats with tannic acid against aluminium chloride exposure was shown to inhibit the production of thiobarbaturic acid reactive substance in erythrocytes lysate and liver tissues, but it failed to inhibit lipid peroxidation in plasma and kideney tissues.
Also it modulated the increase in nitric oxide levels as nitrite in brain tissues, but failed to inhibit that action in plasma and kidney tissues.
Tannic acid also was shown to inhibit the effect of aluminium on antoxidant enzymes; SOD in plasma and brain tissues and catalase in liver and tissues.
Also it preserved glutathione content in liver tissues and the same time, preserved vitamin E content in plasma and brain tissues.
The treatment of rats with tannic acid only for long period induced an elevation in the content of antioxidants; glutathione in kideney tissues and vitamin E in brain and spleen tissues.
Also tannic acid increased the activity of SOD and catalase in spleen tissues.
But, it led to the increase in triglycerides and alkaline phosphatase levels and the inhibition of SOD activity in liver and brain tissues, which might be related to the effect of high dose of tannic acid (50mg/kg of body weight) in the present study.
from the data obtained study aluminium was fround to produce oxidative stress in treated rats by increase the production TBARS and affect in various levels of antioxidant system due to the studied tissue But, the treatment of rats with tannic acid against long-term treatment with aluminium chloride inhibited the toxic action of aluminium on lipid peroxidation and some antioxidants which might be related to the protective effect of tannic acid.
Histopathological changes in liver, kidney, brain and spleen tissues in the present study confirmed the fact that long-term exposure to aluminium chloride induced oxidative damage to the treated animals.
While the improvement of histological pictures after tannic acid treatment might be related to the protective effect of tannic acid.