Average Survival Time

Back ground: Cancer has emerged as the second largest killer disease in the world and mortality rates for solid tumors remain unchanged. Therefore there is need to screen, new remedies to treat cancer. Materials and methods: The antineoplastic activity of different doses of hydroalcoholic extract of Alstonia scholaris (L.) R. Br. (ASE) was studied in Swiss albino mice, transplanted with Ehrlich Ascites Carcinoma cells (EAC) in its peritoneal cavity. The effect of ASE injected at different stages of tumor development was evaluated by studying tumor free survivors. In another study EAC cells were treated with Echitamine Chloride (ECL) in vitro and transplanted back into mice and tumor free survivors determined. The glutathione and lipid peroxidation were also measured after ASE treatment. Results: The daily administration of ASE in tumor bearing mice caused a dose-dependent remission of tumor, and highest regression was observed at 480 mg/kg b. wt. this dose showed some toxic effects and next lower dose i.e. 420 mg/kg was considered as the suitable dose, where 33.33% of the animals survived up to 120 days post-tumor-cell inoculation, as against no survivors in the saline treated control and positive cyclophosphamide treated groups. The ASE caused a dose-dependent elevation in the median survival time (MST) and average survival time (AST), causing a corresponding increase in the median life span (IMLS) and average life span (IALS) of experimental animals. Treatment of EAC mice with 420 mg/kg ASE also retarded tumor development even during the late stages of tumor development, while cyclophosphamide was completely ineffective. The in vitro treatment of EAC cells with ASE or ECL and their transplantation in mice showed that ASE treatment was more potent than ECL treatment as evident by increased MST and AST in the former when compared with the latter. Assay of glutathione and lipid peroxidation after 240, 420 mg/kg ASE or 25 mg/kg cyclophosphamide led to a decline in glutathione contents and increase in lipid peroxidation. Conclusions: Our study shows that ASE treatment kills the tumor cells effectively increasing long-term disease free survival of experimental mice, which may be due to reduced glutathione and increased lipid peroxidation.