1. PENTOSE PHOSPHATE CYCLE
51
is practically nonexistent. In this regard, the transfer of carbon from
lactate to glutamate, aspartate, and alanine occurs rapidly in nontumorous tissues of rats whereas that in tumors is relatively less (339). Thus
the difference in the lactate production by the tumors and the nontumors,
in vivo, may be due not to a difference in the mechanism or the rate of
glycolysis, but rather to the inability of the tumors to convert further
the lactate under the conditions of the experiment.
Needless to say, the variety of tumors is enormous—for each type
of host cell there is at least one kind of neoplastic tissue. Hence it is far
beyond the scope of this review to encompass all aspects of glucose
metabolism by the pentose phosphate cycle in these tissues; most of this
material, anyway, is admirably covered by Alsenberg (338). Suffice it to
say, the principal pathway of carbohydrate metabolism is via the EMP
route and the TCA cycle in mammalian tumors. Katz (111) has estimated that, in the Novikoff hepatoma, between 6 and 8% of the glucose
is metabolized by way of the pentose phosphate cycle, calculated on the
basis of the data of Ashmore et al. (340) and assuming that the metabolism goes solely through the triose pathway with a negligible incorporation into glycogen. These values are apparently fairly typical of many
other tumors. In fact, Table VIII records the relative contribution of the
TABLE VIII
PERCENTAGE OF GLUCOSE METABOLIZED VIA THE PENTOSE PHOSPHATE CYCLE
IN VARIOUS MAMMALIAN TUMORS
% of glucose converted to CCU via
non-EMP pathway
Wenner and Weinhouse Recalculated by Katz°
Tumor
(108)
(111)
TA-3 ascites (mouse)
1 to 2
0
Rhabdomyosarcoma
0 to 2
7
Mammary adenocarcinoma, TA-3,
4 to 16
2
solid (mouse)
Hepatoma (rat)
1 to 7
5
a Assuming that the non-triose pathway is negligible.
pentose phosphate cycle in glucose metabolism in several other types
of tumors. The majority of rat and mouse neoplasms have active pentose
phosphate cycles which scarcely exceed 10% of the glucose metabolized.
The value of 16% obtained by Wenner and Weinhouse represents a
maximum possible value and is probably a more optimistic number.
Some even higher numbers were obtained for the percentages of C0 2
derived from non-EMP pathways: Gardner lymphosarcoma, 32%, and
51
is practically nonexistent. In this regard, the transfer of carbon from
lactate to glutamate, aspartate, and alanine occurs rapidly in nontumorous tissues of rats whereas that in tumors is relatively less (339). Thus
the difference in the lactate production by the tumors and the nontumors,
in vivo, may be due not to a difference in the mechanism or the rate of
glycolysis, but rather to the inability of the tumors to convert further
the lactate under the conditions of the experiment.
Needless to say, the variety of tumors is enormous—for each type
of host cell there is at least one kind of neoplastic tissue. Hence it is far
beyond the scope of this review to encompass all aspects of glucose
metabolism by the pentose phosphate cycle in these tissues; most of this
material, anyway, is admirably covered by Alsenberg (338). Suffice it to
say, the principal pathway of carbohydrate metabolism is via the EMP
route and the TCA cycle in mammalian tumors. Katz (111) has estimated that, in the Novikoff hepatoma, between 6 and 8% of the glucose
is metabolized by way of the pentose phosphate cycle, calculated on the
basis of the data of Ashmore et al. (340) and assuming that the metabolism goes solely through the triose pathway with a negligible incorporation into glycogen. These values are apparently fairly typical of many
other tumors. In fact, Table VIII records the relative contribution of the
TABLE VIII
PERCENTAGE OF GLUCOSE METABOLIZED VIA THE PENTOSE PHOSPHATE CYCLE
IN VARIOUS MAMMALIAN TUMORS
% of glucose converted to CCU via
non-EMP pathway
Wenner and Weinhouse Recalculated by Katz°
Tumor
(108)
(111)
TA-3 ascites (mouse)
1 to 2
0
Rhabdomyosarcoma
0 to 2
7
Mammary adenocarcinoma, TA-3,
4 to 16
2
solid (mouse)
Hepatoma (rat)
1 to 7
5
a Assuming that the non-triose pathway is negligible.
pentose phosphate cycle in glucose metabolism in several other types
of tumors. The majority of rat and mouse neoplasms have active pentose
phosphate cycles which scarcely exceed 10% of the glucose metabolized.
The value of 16% obtained by Wenner and Weinhouse represents a
maximum possible value and is probably a more optimistic number.
Some even higher numbers were obtained for the percentages of C0 2
derived from non-EMP pathways: Gardner lymphosarcoma, 32%, and