الفهرس 
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Abstract
Acesulfame potassium (Ace-K) is one of the commonly used artificial sweeteners, keeping its sweetening property after heating or freezing encouraging its use in various products especially that consumed by children, and encounters a potential hazard for cumulative toxicity. Therefore safety evaluation for its long-term exposure is necessary. A total of 90 mature and immature male Sprague Dawley rats were divided into two main groups, 45 animals each .Immature group subdivided into 3 groups (G1 control untreated, G3&G5 rats treated with Ace-k at a dose of 15 & 90 mg/kg. B.W) and the mature group sub divided also into 3 groups (G2 control group, G4&G6 rats treated with Ace-k at a dose of 15 & 90 mg/kg. B.W), 15 rats per group. All treated rats received Ace-K via gastric intubation daily for 12 weeks. At the end of the experimental period blood samples were collected for the determination of serum amylase, lipase, and glycated hemoglobin and also for testing of lymphocyte proliferation rate, macrophage activity concerning nitric oxide (NO) and the comet assay for isolated lymphocytes. In addition, pancreas and liver were dissected for histopathological evaluation. Liver tissues were collected also for the determination of P53 gene expression. Results revealed that the chronic treatment with Ace-k induced a significant increase in weight gain in younger age-treated groups compared with older ones. Pancreatic enzymes showed non-significant differences between control and treated groups at different ages while a significant reduction in glycated hemoglobin was detected in older age receiving higher doses compared with other treated groups. Ace-k induced modulation in lymphocyte proliferation rate and affected the production of NO by macrophage while increases in the tail moment were detected in the isolated lymphocytes in a dose-dependent manner among different treated groups. Pancreatic histopathological changes were recorded which exhibited a dose-dependent increase in lesion severity among treated groups .In addition, the histological hallmarks of pancreatic pathology induced by Ace-k give attention to the possible carcinogenic potential. Upregulation of P53 in the liver was detected which correlated with increased polyploidization and necro-apoptotic reaction and various histopathological hepatic alterations. Conclusion, the present data revealed that, chronic treatment with Ace-k on rats affected the weight gain, lymphocyte proliferation rate and macrophage activity in a dose-dependent manner. Also, it induced pancreatic injury with attention to possible carcinogenic potential. The genotoxic and hepatotoxic potential of Ace-k were confirmed. So, further studies are essential.