SYSTEMIC INSECTICIDAL ACTION OF NICOTINE AND CERTAIN OTHER ORGANIC BASES

Nicotine and nicotine salts are taken up by the roots of plants from solutions, and when 0.01–0.001 % nicotine is used the plants become toxic to Aphis fabae and to Pieris brassicae larvae and can be shown to contain nicotine. The results with Phaedon cochleariae adults and larvae are less satisfactory. No systemic action is observed when the nicotine is watered on to soil in which plants are growing and no nicotine can be detected in the plants. Apparently the nicotine is decomposed in the soil.
When applied several times to the upper surface of a bean leaf nicotine kills aphids on the underside. There is some evidence that nicotine can be translocated further through the plant following leaf applications, but the toxic action at any distance is very weak in the plants used in the present experiments and can only be produced by frequent applications of rather concentrated nicotine solutions. Leaf absorption and subsequent translocation has not been observed with nicotine salts.
The various organic bases, including some piperidine phosphonites and allied compounds tested, are of very little interest as contact or systemic insecticides against aphids.     

2-Deoxy-D-galactose metabolism in ascites hepatoma cells results in phosphate trapping and glycolysis inhibition.

The metabolism of 2-deoxy-D-galactose has been studied in AS-30D rat ascites hepatoma cells in suspension. Using 2-deoxy-D-(1-14C)galactose and an alkaline ethanol deproteinization procedure, the quantitatively identified metabolites included 2-deoxy-D-galactose 1-phosphate comprising 99.3%, and UDP-2-deoxy-D-galactose and UDP-2-deoxy-D-glucose, together amounting to 0.4% of the total metabolites. After incubation for 5 h in the presence of 2-deoxy-D-galactose (1 mmo1/1), the content of 2-deoxy-D-galactose 1-phosphate reached 35 mmo1x(kg cells)-1. The rate of phosphorylation of 2-deoxy-D-galactose was rapid during the first 30 min and decreased to approximately 20% of this rate during the subsequent hours. The rapid trapping of Pi in the form of 2-deoxy-D-galactose 1-phosphate resulted in a depression of free intracellular Pi in spite of a concomitant increase in net 32Pi uptake from the medium and a decrease of ATP and other 5'-nucleotides. The rates of glucose utilization and lactate production were depressed by more than 80% in the presence of 2-deoxy-D-galactose (1 mmo1/1). Interruption of Pi trapping by removal of 2-deoxy-D-galactose from the medium reversed the depressions of Pi and ATP and resulted in a rapid but incomplete relief of glycolysis inhibition. Crossover analysis of glycolytic intermediates indicated an inhibition at the 6-phosphofructokinase step. The depression of glucose utilization may be mediated by the increased level of glucose 6-phosphate, a potent inhibitor of hexokinase. An additional inhibitory effect of a metabolite of 2-deoxy-D-galactose at the 6-phosphofructokinase step was indicated by crossover analysis after reversal of Pi and ATP depressions in the presence of a high intracellular content of 2-deoxy-D-glactose 1-phosphate. The quantitative analysis of the metabolites of 2-deoxy-D-galactose demonstrated the predominance of the monophosphate and the negligible formation of UPD derivatives of this sugar analog in AS-30D hepatoma cells. This provides a system for the investigation of a galactose analog as a phosphate-trapping agent in the virtual absence of uridylate trapping.