23 5 vasan(l0). Our values with normal rats, however? compared favourably with theirs. Tn their case a decrease in nl-globulin wit.h significant increase in ,%globulin was observed, whereas under our conditions an increase in az-globulin with a decrease in yglobulin was observed.Summary. Different fractions of serum proteins were determined by paper electrophoresis in folic acid deficient and pair-fed normal rats. Total serum protein was low and plasma fibrinogen was significantly high in the deficient animals. There was a significant decrease in albumin and 7-globulin, considerable increase in aa-globulin, with no significant change in al and p-globulin fractions in the serum of folic acid deficient rats, Aminopterin was kindly supplied by Lederle Lab. (India). -1. Dinning, J. S., Day, P. L.,

A previous publication (Rogers and Mahan, '59) has described the exchange of radioactive magnesium in various tissues of the rat. It was found that there are two principal exchange rates, one with a turnover time of 1.2 hours and another with about 25 hours. In myocardium, liver and kidney, only the fast component was apparent and the specific activity of the tissue magnesium reached that of the plasma magnesium in three hours. In the other tissues studied (brain, skeletal muscle, testes and red cells), more than half of the magnesium exchanged at the slower rate. It was of interest to compare the exchange of radioactive magnesium in the red cells of other species both in vivo and in vitro, and in rat cells in nitro. METHODSFor the in vivo studies, isotonic solutions of MgC1, containing Mg" were injected i/v into dogs and cats. Blood samples were drawn at intervals from the catheterized femoral artery. In the in vitro studies, the radioactive solution was added to whole blood of rats, dogs, cats, cattle and man, which was then incubated at 38°C with gentle agitation under 5% carbon dioxide in oxygen. Samples were drawn at intervals.In each case, the blood was immediately centrifuged at a standard rate for 4 minutes and the plasma removed for radioactive and chemical assay. The cells were washed with ice-cold isotonic saline, centrifuged for 4 minutes and then the washing and centrifugation were repeated once more. An aliquot comprising 0.5 ml of washed, packed red cells was added to 0.5 ml water in a tube which was then placed in a well-type scintillation counter. After counting, 2 ml of 10% trichloracetic acid was added to the hemolysate and centrifuged in the same tube. The supernatant fluid was analyzed for magnesium by the method of Orange and Rhein ('51). Plasma samples received similar treatment. The results are expressed as the "relative specific activity" (r.s.a.) which is the ratio Specific activity of red cell Mg Specific activity of plasma MgWhen this ratio is equal to 1.0, equilibration is complete. An advantage of this method of expressing the data is that variations in the packing of the cells are unimportant because the count rate and magnesium content are determined for each 1 ml sample of hemolysate. In some instances the hemolysate was centrifuged and the supernatant counted (without the cell ghosts). In each case the count rate was identical with that in the original sample, indicating that the Mgz* content of the "membranes" was negligible. RESULTS AND DISCUSSIONThe in vivo and in vitro equilibration of the magnesium in cat red cells with that in the plasma is shown in figure 1; almost identical curves were obtained for dog and rat cells. The pattern of equilibration in rat erythrocytes in vivo, which was previously described (Rogers and Mahan, '59), was determined by sacrificing isotopeinjected animals in series. All the results obtained in vivo tend to lie on less smooth curves than those in vitro and this may be partly attributed to the rapid biological decay of the plasma magnesium radioac...

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The effects of physiologic acids on muscle electrolytes were studied by incubating rat hemidiaphragms in Krebs-Ringer solution or blood at pH 7.4 and 6.8. With the addition of acetic, lactic or beta-hydroxybutyric acid to depress the pH, the sodium and potassium contents of muscles incubated in Krebs-Ringer solution were the same at each pH. This is in contrast to the efflux of these cations previously observed on adding hydrochloric acid to this medium. Using heparinized rat blood as the medium, the effect of hydrochloric acid was the same as in Krebs-Ringer solution. With acetic acid however, the pattern was reversed. Muscles in blood acidified with acetic acid actually retained more potassium than the controls at pH 7.4. An increased Pco2 to depress the pH in blood did not affect the potassium content, but there was a gain of sodium in the muscles in the more acid blood so that the net cation content increased. In contrast to the physiologic acids which can penetrate the cells as intact molecules, hydrochloric acid produces an essentially extracellular acidosis. Hydrochloric acid therefore causes a displacement of intracellular cation as hydrogen ions penetrate the cell. With blood, which is better buffered than the intracellular fluid, acetic acid and carbon dioxide depress the intracellular pH more than the extracellular pH. The pH gradient across the membrane is then analogous to that with hydrochloric acid but in the opposite direction resulting in a movement of cations into the cells.

Metabolism of C14 fructose has been studied in dairy cows and the results compared to those obtained earlier with C14 glucose. C14 fructose disappeared rapidly from the plasma; simultaneously there occurred an immediate rise in plasma glucose C14. The pattern of isotope distribution in milk C and the peak expired CO2 specific activity was the same after fructose as after glucose injection. These results suggest that glucose is a key intermediate in the metabolism of fructose—the conversion of fructose to glucose presumably occurring in the liver. That fructose is also metabolized to a considerable extent by other pathways was indicated by the earlier peak—and more rapid decline—in expired CO2 specific activity. Further, considerably less fructose C14 was found in expired CO2 and in milk C 24 hours after injection. The extent to which fructose was metabolized by pathways which did not involve plasma glucose was estimated by comparing the integrated specific activity/time curves after fructose and glucose injection. It appears that up to 50% of the transfer of fructose C to expired CO2 and to milk C goes by pathways exclusive of blood glucose.