In order to compare the efficacy of sinigrin with a common cancer drug, doxorubicin was used to treat the carcinogensinduced hepatocarcinogenesis in the rat. The results showed that after doxorubicin treatment the number of surface tumors in the rat liver was not affected whereas the group of rats that was treated with sinigrin displayed considerably reduced numbers of surface tumors. The liver weight index of doxorubicin-treated group was similar to that of the positive control group. The histological changes of liver section from rats were examined. The results indicated that there were obvious histological changes between treated and the untreated groups of rats. The liver sections from doxorubicin-treated rats displayed similar structures to those of the positive control groups of rats. These results on histological Folinic acid calcium salt pentahydrate change suggest that doxorubicin was not effective at altering carcinogen rats at this stage of tumor development. The liver sections of different control and treatment groups of rats were also analyzed with GST-p antibodies. The results 
of GST-p antibody labeling of the assorted liver sections provide supportive experimental evidence that rat liver functions could be restored after treatment with sinigrin relative to the negative control and the positive groups of rats. The GST-p foci showed clearly that doxorubicin treatment was ineffective managing or attenuating carcinogen-induced hepatocarcinogenesis. The levels of the rat liver enzymes ALT and AST were, importantly, significantly decreased. These data suggest that liver functions can be gradually restored after treatment with sinigrin. At the molecular level, an attempt was made to understand possible changes in gene expression associated with sinigrin treatment. The results, as indicated in Figure 9, revealed profound changes in the levels of p53 mRNA in rats following treatment with sinigrin. This change reflects the likelihood that sinigrin induces apoptosis via a p53-dependent pathway. Notably, levels of MDM2 mRNA in the sinigrin treatment group also were considerably higher than in the negative control group. This change in MDM2 expression was accompanied by alterations in the gene expression of Bax, Bcl-2 and PCNA. These findings suggest that sinigrin exerted anti-proliferative activity carcinogen-induced liver damage in the rat, and caused cell cycle arrest and amelioration of liver functions in the rat. The anti-proliferative activity of sinigrin was increased with increasing dosages. The present findings demonstrate that sinigrin is an excellent glucosinolate with medicinal properties, and add to the literature on bioactive phytochemicals in cruciferous vegetables, especially glucosinolate compounds that can inhibit the growth of liver cancer cells; such information pertaining to the anticancer activity of the glucosinolates endogenous to Brassica is limited. Sinigrin was shown to Clofentezine possess anti-cancer activities in the present study. The cell cycle analysis indicated that sinigrin caused cell cycle arrest in G0/G1 phase. Sinigrin triggered the release of cytochrome c through the down-regulation of Bcl-2 and up-regulation of Bax. The present findings reveal that Bcl-2 protein expression was significantly lower in the sinigrin treated group of rats than in the positive control group. Bax was overexpressed in the negative control and the sinigrin-treated groups relative to the positive control group. These results suggest that the over-expression of mutant p53 was increased in the rat after carcinogen exposure and subsequent carcinogenesis. The major regulator of p53 turnover, Mdm2 was found to be over-expressed at the transcriptional level in the untreated positive controls. The over-expression of Mdm2 is associated with the wild-type p53 degradation.