A diet containing the lectin phytohaemagglutinin (PHA) slows down the proliferation of Krebs II cell tumours in mice.

Mice injected intraperitoneally with Krebs II cells and then fed on a diet containing the lectin phytohaemagglutinin (PHA) developed ascites tumours more slowly than mice fed on a control diet. After an 8-day period following injection the number of cells recovered from mice maintained on the PHA diet was half that from those fed the control diet. A switch of diet from control to PHA on day 4 after injection resulted in a large decrease in number of tumour cells recovered. Mice injected s.c. also developed tumours at later times when fed on the PHA diet. A quantitative of ribosomes in polysome-containing fractions showed no major differences in protein synthesis in control mice and those fed the PHA diet.

Dietary phytohaemagglutinin slows down the proliferation of a mouse plasmacytoma (MPC-11) tumour in Balb/c mice.

Ten days after subcutaneous injection of MPC-11 cells, plasmacytoma tumours which developed in female Balb/c mice fed on a diet containing the kidney bean lectin phytohaemagglutinin (PHA) at a concentration of 7.0 mg g-1 diet, weighed only about 38% of those fed a lactalbumin (La) control diet. The reduction in growth caused by the lectin appeared to occur in a dose-dependent manner but the values did not reach significance before PHA was at a concentration of 7.0 mg g-1 diet. Pre-feeding with the lectin caused a further 50% reduction in tumour weight. In contrast to the reduction in tumour size the inclusion of PHA in the diet elevated the mean dry weight of the small intestine in a dose-dependent manner, values reaching significance at 3.5 mg g-1 diet. The results showed that gut hyperplasia was able to occur even in the presence of the developing tumour. A lypolytic effect of PHA occurred at high concentration. The observations suggest that PHA itself does not have a direct effect on the tumour cells, but an inter-relationship between gut hyperplasia and decreased tumour growth is indicated.

Phytohemagglutinin-induced gut hyperplasia and the growth of a mouse lymphosarcoma tumor.

NMRI mice injected subcutaneously with Krebs II lymphosarcoma cells and fed on a diet containing the kidney bean lectin phytohemagglutinin (PHA) within the range 0.45-7.0 mg/g diet, developed tumors during a 10 day period which on average were only 35% of the dry weight of tumors in lactalbumin (La) fed mice (control). The reduction in growth occurred in a dose-dependent manner in the range 0.45-3.5 mg/g diet. The degree of hyperplasia of the small intestine in response to feeding the PHA diets was higher in non-injected compared to injected mice. A lipolytic effect of PHA was observed above 1.75 mg/g diet in control mice and the highest concentration had a major effect on body weight. Since the index of hyperplasia at the lowest PHA concentration tested did not correlate with the reduction in tumor size, it is suggested that other factors in addition to the initial lectin-induced gut hyperplasia are involved in slowing down the progression of tumor growth.

The effect of switching between a phytohemagglutinin-containing and a control diet on the growth and lipid content of a Krebs II lymphosarcoma tumor.

The present study concerns the importance of the timing of feeding mice a PHA-containing diet (7 mg g-1 diet) on tumor formation. The major decrease in tumor weight occurred in mice fed on the PHA diet for 11 days. A marked reduction was also observed in animals pre-fed for 3 days with PHA before tumor cells were injected and the diet then changed to lactalbumin, La. A large decrease in tumor weight was also evident when a change of diet from La to PHA was made on the day of tumor cell inoculation. Despite the presence of the developing tumor PHA was able to induce hyperplasia of the small intestine in all groups of animals fed PHA during a part or the whole of the experiment. The dry weights of tumors attained in each of the experimental groups plotted as a function of duration of PHA feeding, and the percentage lipid content of the tumors, mirrored almost exactly one another, suggesting that the availability of essential lipid material is severely reduced by the lectin. This would appear to have a major effect on the observed reduction in tumor growth.