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Tissue Nitrogen-sparing Effect of High Protein Diet in Mice with or without Ascites Tumor Treated with Acinetobacter Glutaminase-Asparaginase¹

Departments of Medicine, Pediatrics, and Biochemistry, School of Medicine, West Virginia University, Morgantown, West Virginia [C. L. K.]; Department of Medicine, Medical College of Wisconsin, Milwaukee, Wisconsin [A. J. A.]; and the Department of Pediatrics, School of Medicine, University of Southern California, Los Angeles, California [J. S. H.]

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% NaCI 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 < 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 < 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 < 0.01) (compared to NP) but HP resulted in percentage increases in the nitrogen content of liver (18%; P = 0.05), intestine (25%; P < 0.05), and thymus (164%; P < 0.01). In the Ehrlich ascites tumor, AGA group the HP diet caused higher hematocrit and serum total protein (both, P < 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.

¹ This study was supported in part by NIH Grant CA 20061, The Burroughs Wellcome Foundation and the Midwest Athletes Against Childhood Cancer. Portions of this work were presented at the Annual Meetings of The Society for Pediatric Research (5/3/84, San Francisco and 5/5/83, Washington, DC), and FASEB (4/3/84, St. Louis).

² Recipient of a Future Leader's Award from the Nutrition Foundation, Inc., and Special Fellow of the Leukemia Society of America, Inc., while these studies were being conducted. To whom correspondence should be addressed, at Section of Clinical Nutrition, Department of Medicine, West Virginia University, Medical Center, Morgantown, WV 26506. Reprints will not be available.

Received 4/23/84. Revised 6/26/85. Accepted 7/ 2/85.

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