These findings suggest that sinigrin down-regulates the expression of Mdm2 thus leading to an increase in p53 expression. The over-expression p53 presumably enhances expressions of Bax, Bcl-2 and p21 leading to cell cycle arrest and apoptosis. Notably, the positive control group of rats was found to show a considerable increase in PCNA expression whereas the sinigrin-treated rats showed a decrease in PCNA expression. This suggests that liver cell proliferation was attenuated by subjection to sinigrin. These findings suggest that liver damage related to carcinogen triggered carcinogenesis was remarkably reduced in rats following exposure to sinigrin. Indeed, the histological changes observed between different treatment groups and the negative control groups reveal that sinigrin appears to attenuate carcinogen-triggered liver injury in the rat. Histological changes in liver sections from the treated groups of rats suggest that sinigrin suppresses the formation of preneoplastic foci due to carcinogen exposure. Gross examination of the liver from the positive control rats showed the presence of lipid droplets, nodules and tumors across the surface of the rat liver. Histological examination of rat liver sections revealed that hepatocytes of sinigrin -treated rats appeared to display the cuboidal shape that is characteristic of normal hepatocytes. These findings demonstrate that sinigrin exhibits anti-cancer properties in the rat on a dosage dependent manner. The health benefits of sinigrin was confirmed when a higher dose of sinigrin was used. The results suggest that the anti-cancer activity of sinigrin is attributed to the radical scavenging capacity of sinigrin which is believed to play an important role in ameliorating liver damage. The ratio of liver weight and body weight serves as a representative marker of the anti-oxidative capacity of the liver. A decrease in ALT and AST suggests risk reduction for oxidative damage. Salvianolic-acid-B Alterations in the enzyme levels for ALT and AST are common features of oxidative stress and pathological conditions associated with liver damage. Reductions of ALT and/or AST levels are important for instilling protection from carcinogeninduced liver damages. In the present study, we showed that treatment with sinigrin remarkably decreased the GST-p foci which were greater than those observed for the untreated group and the doxorubicin-treated group. This suggests that sinigrin possesses anti-cytotoxic activities in carcinogen-induced liver injury. Previous studies have revealed that cells differ in their response to carcinogens depending on their levels of p53 activity. Activation of p53 in liver cells resulted in up-regulation of p21 and to increased expression of Bax and, proapototic Bcl-2 activities leading to mitochondrial pore opening. Both p53 and p21 protein levels were also increased. The activation of p53 plays a crucial role in sinigrin-induced down-regulation of Bax, Mdm2 and Bcl-2 family members highlighting that a functional p53 is required for the execution of apoptosis in cancer cells. It is known that p53 regulates the cell cycle and apoptosis by activating expression of target proteins including Mdm2, p21, PCNA, Bcl-2 and Bax. Mdm2 is associated with the regulation of p53 turnover. The over-expression of Mdm2 protein likely enhances degradation of more wild type p53 protein. Importantly, Mdm2 was found to be over-expressed in the positive control group whereas the expression levels of Mdm2 were downregulated in sinigrin-treated cells relative to the positive control. These results suggest that sinigrin is capable of down Cinoxacin regulating the critical regulator Mdm2. In a related fashion, increases in p21 are known to be related to the inactivation of PCNA.