Search

The presence of putrescine or chlorpheniramine in the incubation medium of Ehrlich ascites tumor cells starved for 1 h significantly inhibits the rate of ferricyanide reduction by their plasma membrane redox system. Freshly harvested cells, without depletion of their intracellular pools of polyamines, and cells preincubated under conditions arranged to increase ornithine decarboxylase activity also reduced externally added ferricyanide at a lower rate than those cells starved for 1 h. All these data seems to indicate that the presence of putrescine is enough to significantly inhibit Ehrlich cell plasma membrane redox system activity.

The biological effects of dehydrodidemnin B(DDB), a novel depsipeptide isolated from Aplidium albicans, were studied on Ehrlich carcinoma growing in vivo and in primary cultures, and compared with those reported for Didemnin B (DB). Daily administration of DB or DDB (2.5 micrograms/mouse) almost duplicated the animal life-span and total number of tumour cells decreased by 70-90%. Results suggest a major effect of DDB when administered in the lag phase of growth. DDB behaved as a very potent inhibitor of protein synthesis; consequently, ornithine decarboxylase activity (ODC, EC 4.1.1.17) is drastically reduced by DDB-treatment.

Naturally occurring vinca alkaloids, vincristine and vinblastine, at micromolar concentrations enhanced the ornithine decarboxylase activity in a dose-response manner in primary cultures of Ehrlich ascites carcinoma cells. After 8 h of culture in the presence or absence of vinblastine, cycloheximide was added to the medium, a 4.5-fold increase in the half-life of the ornithine decarboxylase activity was observed in vinblastine-treated cells. This effect is probably due to the inhibition of the intracellular enzyme degradation by the vinca alkaloids.