effects of treatment with platinum azidothymidine and azidothymidine on telomerase activity and bcl-2 concentration in hepatocellular carcinoma- induced rats

background: telomerase activity increases in cancer cells. bcl-2 is an antiapoptotic factor that its concentration grows in many cancer cells including hepatocellular carcinoma cells. in this study, an attempt was made to investigate the effects of a new synthetic compound, platinum azidothymidine (pt-azt) on treatment of rats with hepatocellular carcinoma (hcc) and to compare its effects with azidothymidine (azt) in alteration of telomerase activity and bcl-2 concentration in hcc. methods: healthy adult male wistar rats (n=100) were randomly divided into 4 groups (a, b, c, and d). group a contained 25 healthy rats and was considered as the control group. liver preneoplastic lesions were induced in remaining animals (n=75) using solt-farber resistant hepatocyte protocol. these animals were randomly allocated in groups b, c and d. group b was negative control (untreated), groups c and d were treated by intraperitoneal injection (ip) of pt-azt (0.9 mg/kg/day) and azt (0.3 mg/kg/day), respectively for 14 days. after the treatment period, telomerase activity and bcl-2 concentration were determined in the rats’ liver. results: no hcc was developed in group a, but tumors were present in all other groups. telomerase activity and bcl-2 concentration were significantly lower in group c compared to groups b (0.1590.06 vs. 0.5770.116 iu/l, p<0.001, respectively and 0.9310.388 vs. 3.940.74 ng/ml, p<0.001, respectively). similar results were observed in comparison with group d (0.3310.06 vs. 0.5770.116 iu/l, p<0.001, respectively and 0.9310.388 vs. 2.940.594 ng/ml, respectively). there was a significant negative correlation between telomerase activity and bcl-2 concentration only in untreated cancer group (p=0.034). conclusion: in this study, higher anticancer activity of pt-azt in comparison to azt was demonstrated. it effectively inhibits the growth of liver tumor in rats through extending apoptosis.