PURPOSE: Chemoprotective effect of diphenylmethyl selenocyanate against cyclophosphamide (CP) induced cellular toxicity and antitumor efficacy was evaluated in mice bearing Ehrlich ascites carcinoma. METHODS: Diphenylmethyl selenocyanate (3 mg/kg.b.w.) was administered orally and CP was given intraperitoneally (25 mg/kg.b.w). The effects were observed on the level of lipid peroxidation, antioxidant enzymes status, serum transaminase (ALT, AST) activity, hematological profile, transplantable murine tumor growth, apoptosis induction in tumor cells, and life span of tumor bearing hosts. RESULTS: The selenium compound restored the levels of antioxidant enzymes system, decreased the level of lipid peroxidation and serum transaminase activity. Hematological profile reverted to near normal level after selenium compound treatment. Treatment with the selenium compound also resulted in significant tumor growth regression along with significant upregulation of apoptosis, increased in mean survival time and life span of tumor bearing host. CONCLUSIONS: Results clearly indicate that diphenylmethyl selenocyanate has the potential to reduce the cellular toxicity of CP at the same time improving its antitumor efficacy.
PURPOSE: Chemoprotective effect of diphenylmethyl selenocyanate against cyclophosphamide (CP) induced cellular toxicity and antitumor efficacy was evaluated in mice bearing Ehrlich ascites carcinoma. METHODS:Diphenylmethyl selenocyanate (3 mg/kg.b.w.) was administered orally and CP was given intraperitoneally (25 mg/kg.b.w). The effects were observed on the level of lipid peroxidation, antioxidant enzymes status, serum transaminase (ALT, AST) activity, hematological profile, transplantable murinetumor growth, apoptosis induction in tumor cells, and life span of tumor bearing hosts. RESULTS: The selenium compound restored the levels of antioxidant enzymes system, decreased the level of lipid peroxidation and serum transaminase activity. Hematological profile reverted to near normal level after selenium compound treatment. Treatment with the selenium compound also resulted in significant tumor growth regression along with significant upregulation of apoptosis, increased in mean survival time and life span of tumor bearing host. CONCLUSIONS: Results clearly indicate that diphenylmethyl selenocyanate has the potential to reduce the cellular toxicity of CP at the same time improving its antitumor efficacy.