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Surgical Metabolic Research Laboratory, Department of Surgery, [K. L., I. K., L. E., T. S.], and Department of Oto-Laryngology [S. E.], Sahlgrenska Sjukhuset, University of Göteborg, Göteborg, Sweden
Reutilization of amino acid carbons was evaluated in relation to increased turnover of albumin in tumor-bearing mice.
A methylcholanthrene-induced sarcoma (MCG 101) was used in nongrowing mice (C57BL/6J).
Sarcoma-bearing mice developed hypoalbuminemia, but pair-fed controls did not. The hypoalbuminemia was caused by increased albumin degradation rate, measured by injection of Na214CO3, and by exponentially increased deposition of albumin into the tumor compartment. The fractional synthesis rate of albumin was doubled in tumor-bearing mice compared with controls. The translational capacity of albumin synthesis evaluated in vitro was maintained in tumor host livers. The recycling of [14C]leucine carbons was almost extinguished in plasma albumin of sarcoma-bearing mice, while that of control mice contributed to 30 to 40% of the total leucine carbon flux in turned over albumin. The recycling of arginine carbons was also different when measured after simultaneous injection of [guanido-14C]arginine and [2,3-3H]arginine. The hepatic pool of free leucine was increased by 22% in tumor-bearing mice.
It is concluded that increased albumin degradation in cancer may be a disordered event and is earlier and of initially greater quantitative importance than is altered synthesis of albumin for the development of hypoalbuminemia in experimental cancer.
1 This work was supported by grants from the Swedish Cancer Society (Project 93), the Swedish Medical Research Council (Project 536), the Assar Gabrielsson Foundation, and the Serena Ehrenström Foundation.
2 To whom requests for reprints should be addressed: Department of Surgery I, Sahlgrenska Sjukhuset, 413 45 Göteborg, Sweden.
Received 12/ 8/80. Accepted 2/10/82.
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