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Hexokinase isoenzyme type I was purified from various rat tissues, and was subjected to kinetic studies in the presence or the absence of p-chloromercuribenzenesulphonate. The mode of the inhibition by the thiol inhibitor was different for the type I isoenzymes obtained from different tissues, suggesting that the type I isoenzymes from different tissues were not identical proteins.

After the injection of radioactive strontium, a mixture of trisodium citrate and monosodium monocalcium citrate was injected into rats and the effect of monosodijm monocalcium citrate injection in accelerating the excretion of radiostrontium was compared with the effect of the injection of trisodium citrate only. Greatly enhanced excretion of radiostrontium into urine was found in the rats treated with sodium calcium citrate, without any symptom of hypocalcemia. When citrate was injected into rats in the form of either trisodium salt or sodium calcium salt, citrate level in blood plasma was greatly elevated and nearly one-half of injected citrate was found in the urine within six hours. Mechanism of the action of citrate on the excretion of radioactive strontium is discussed and attributed to its chelating ability.

The mechanism of insulin action on hexokinase isozymes was examined by the electrophoresis on cellulose acetate membrane. It is demonstrated that insulin, some (receptor) protein and type II may form a complex sensitive to sulfhydryl compounds, which appears as type III in some tissues, or as the abortive one with disappearance of type II in others. On this mechanism insulin was deduced to act to induce the protein for the complex as well as to form this complex as a constituent.

Decrease in Type II and concomitant increase in Type III in the hexokinase isoenzymogram of rat carrageenin granuloma were induced in vitro by the addition of insulin to the incubation medium. The changes in the isoenzymogram observed in vitro were quite similar to those induced by insulin in vivo in the same tissue. Addition of pchloromercuribenzene sulfonic acid, a sulfhydryl inhibitor, to the medium also caused decrease in Type II. On the other hand, Type II was markedly increased by the addition of mercaptoethanol, a sulfhydryl compound, to the isoenzyme solution. The findings were discussed with respect to the mechanism of the effect of insulin, especially on the relation between insulin action and state of sulfhydryl groups in the experimental system.

Sodium tricarballylate (8.5 m.mole/kg.) activates the excretion of radioactive strontium injected and reduces its skeketal accumulation. Under a similar condition, sodium lactate (13.5 m.mole/kg.×4) is ineffective. Mechanism of active excretion caused by the injection of tricarballylate was discussed and suggested to be due to its chelating action. Some side effect of tricarballylate injection was observed but it did not produce severe injury.

Effect of tricarballylate, citraconate, tartrate, lactate, and citrate, which are able to form chelating complex with strontium, on the distribution of parenterally administered radioactive strontium was examined, and it was indicated that all of these organic acids markedly decreased skeletal depostion of radiostrontium and four acids other than citrate markedly increased radiostrontium in the blood serum and soft tissues.