Abstract
The effects of α-ketoglutarate (α-KG) on hyperammonemia induced by ammonium acetate were studied biochemically in experimental rats. The levels of circulatory urea and non-protein nitrogen increased significantly in rats treated with ammonium acetate and decreased significantly in rats treated with α-KG and ammonium acetate. In liver and kidney tissues, similar patterns of alterations across groups were observed in the levels of thiobarbituric acid-reactive substances and lipid profile variables (free fatty acids, triacylglycerols, phospholipids, and cholesterol). Further, enzymatic (superoxide dismutase, catalase, and glutathione peroxidase) and non-enzymatic (reduced glutathione) antioxidants in both tissues decreased significantly in rats treated with ammonium acetate and increased significantly in rats treated with α-KG and ammonium acetate. The biochemical alterations during α-KG treatment might have been due to 1) the detoxification of excess ammonia, 2) participation in the non-enzymatic oxidative decarboxylation during hydrogen peroxide decomposition, and 3) enhancement of the proper metabolism of fats that could suppress oxygen radical generation and thus prevent lipid peroxidative damages in rats.
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