Forty-eight
tumor-free mice and 32 mice bearing
Ehrlich ascites tumor were randomized into 2 treatments, Acinetobacter
glutaminase-asparaginase (AGA) (600 IU/kg/day for 7 days) and
0.9% NaCl controls, and into 2 or 3 isocaloric diets, normal
protein (NP) (20
g protein/100 g
diet), high protein (HP) (58
g protein/100 g diet), and zero
protein (ZP) (
tumor-free mice only). In
tumor-free, NP-fed mice, AGA caused percentage reductions (P less than 0.01) in the
nitrogen content of liver (50%), intestine (42%), thymus (89%), spleen (75%), and carcass (20%), but HP prevented this effect on intestine and carcass and caused percentage increases in the
nitrogen content of liver (53%), intestine (36%), thymus (122%), and carcass (25%). In
Ehrlich ascites tumor mice (NP or HP fed) AGA caused markedly lower (P less than 0.01)
tumor burdens and increased
nitrogen content of intestine (HP), kidney (NP and HP), and spleen (NP and HP).
Ehrlich ascites tumor, AGA-treated, HP-fed mice ate 31% less food (P less than 0.01) (compared to NP) but HP resulted in percentage increases in the
nitrogen content of liver (18%; P = 0.05), intestine (25%; P less than 0.05), and thymus (164%; P less than 0.01). In the
Ehrlich ascites tumor, AGA group the HP diet caused higher hematocrit and serum total
protein (both, P less than 0.05). Adverse nutritional effects of AGA seen in normal mice were markedly diminished in
tumor-bearing animals. The observed
nitrogen-sparing effects of the high
protein: energy ratio may be relevant to humans and to other forms of
neoplasia and
chemotherapy.