394 G. ROUSER, A. J. SAMUELS, D. HELLER, B. JELINEK 
compounds and glutamine is relatively low. This pattern was not characteristic 
either for this particular patient or for the disease in general. 
Figs. 130 and 131 illustrate the free amino acid pools of lymphoblasts obtained 
on two different occasions from a patient (R. Can. 3) with acute lymphoblastic 
leukemia. Of particular interest is the extremely low level of glutamine and the very 
low level of alanine compared to other types of normal or leukemic cells. As shown 
in Fig. 132, myeloblasts obtained from a patient (C. Ver. 3) with acute myeloblastic 
leukemia are similar to the lymphoblasts in having an extremely low glutamine 
level but differ in that the alanine level is very high in myeloblasts. The myeloblasts 
have a larger free amino acid pool and glutathione is undetectable in these cells. 
CONCLUSIONS 
It can be concluded that untreated patients with chronic lymphatic leukemia tend 
to show a lower than normal plasma glutamine level and on occasions an elevated 
plasma glutamate level. Other free amino acids are usually within the normal range 
in the untreated patients. 
No characteristic changes specific for chronic lymphatic leukemia or consistent 
differences from normal were observed for plasma, red cell, or urine free amino acid 
levels. 
The most characteristic findings were with respect to the free amino acids of the 
leukocytes. Leukocytes from some patients showed very low levels of glutamine. 
The glutamine level was particularly low in cells obtained from bone marrow aspirates. 
The leukocytes from different patients showed significantly different free amino acid 
patterns. This is in spite of the fact that the cells were similar morphologically. 
Although marked deviations from the normal patterns were observed in plasma, 
erythrocytes, and urine of patients with acute leukemia, the significance of these 
changes could not be assessed as the patients required treatment. These studies 
were not pursued to the point where definite conclusions could be drawn. It is evident, 
however, that both lymphoblasts and myeloblasts from patients with acute lympho- 
blastic and myeloblastic leukemia show very low levels of glutamine and that the 
peripheral blood leukocytes obtained from patients with acute monocytic, acute 
lymphoblastic, and acute myeloblastic leukemia are distinctly different and can be 
recognized readily by their free amino acid patterns. The cells from the monocytic 
leukemia patient contained much more glutamine than cells from acute lympho- 
blastic and myeloblastic leukemias. 
It is difficult to compare the findings of the present study with those of MCMENAMY 

Fig. 127. Shows the free amino acids from 0.5 ml] of urine of the patient with monocytic leukemia 
to show the marked elevations of the leucines, valine, and histidine (indicated by arrows from 
above downward). 
Pigs. 128 and 129. From extracts of 0.5 ml and 1.0 ml of erythiocytes from the patient with 
monocytic leukemia and a patient with an acute blastic leukemia to show some of the deviations 
from normal. The arrow in Fig. 128 points to uncharacterized compounds, while the ar1ows in 
lig. 129 indicate, from left to right, the relatively high level of glutamic acid, aspartic acid, and 
glutathione. 
Figs. 130-132. From extracts of 100 mg of leukoyctes from a patient with acute lymphoblastic 
leukemia (130 and 131) and myeloblasts from peripheral blood of a patient with acute myelo- 
blastic leukemia (Fig. 132). For abbreviations see p. 369. 
References p. 447/448 
