Cytocidal and toxic effect of various cytostatic drugs on three ascites tumors of the mouse

Abstract

The cytocidal and toxic effects of four cytotoxic drugs (CY, DDP, VCR, Ara-C) were studied using three types of ascites tumors (L 1210, JB-1, EAT) growing on three different mouse strains (B6D2F1, AKR, NMRI). There were considerable differences in the cytocidal effect of the same dose of each drug on the three tumor cell lines; 100% of the L 1210 ascites tumor-bearing animals were permanently cured by a high dose of CY (300 mg/kg) and 30% by DDP (13 mg/kg), while most of the JB-1 and all EAT-bearing mice died earlier than the untreated control mice. The sensitivity of the animals of the three mouse strains to the toxic effect of the same drug dose also differed. CY was better tolerated than DDP. Ara-C and VCR doses used in the present work were non-toxic and showed little cell killing effect. Furthermore, the present study showed that tumor-bearing mice were more sensitive to the toxic side effects of CY, DDP, and Ara-C than tumor-free animals. The growing tumor itself increased the vulnerability of normal cells to the drug.

Mitoxantrone treatment of murine myeloid leukaemia sublines

“…The results of the study comparing the responses of normal mice and leukaemia-bearing mice to treatment with identical doses of mitoxantrone appear to indicate that the latter are more susccptible to the toxic effects of mitoxantrone than the former. A similar effect has also been reported for cytosine arabinoside (Schafer and Maurer-Schultze, 1987). In BNML leukaemic rats, the factors responsible for early deaths may include excessive cell killing leading to tumour-cell embolism in association with impaired function of vital organs by leukaemic cells (Hagenbeek and Martens, 1982).…”

“…A similar effect has also been reported for cytosine arabinoside (Schafer and Maurer-Schultze, 1987). In BNML leukaemic rats, the factors responsible for early deaths may include excessive cell killing leading to tumour-cell embolism in association with impaired function of vital organs by leukaemic cells (Hagenbeek and Martens, 1982).…”