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( University of Texas M. D. Anderson Hospital and Tumor Institute, Department of Biochemistry, Houston, Texas)
The mechanism of tumor glycine and serine biosynthesis from nonamino acid precursors was studied, with carbon-14-labeled acetate, glucose, ribose, and formate as substrates. The conversion of acetate-2-C14 to glycine by the Gardner ascites tumor was markedly inhibited by glucose, serine, fluoride, and malonate, but not by hydroxypyruvate or glycollic acid. Radioactivity was also observed in free serine.
After incubating tumor cells with glucose-6-C14 or glucose-1-C14, serine, but not glycine, was labeled. Serine and glycine were both labeled when glucose-2-C14 was used. In the presence of fluoride and pyruvate, the radioactivity of serine was increased but that of alanine was reduced.
Some labeled glycine was formed by lymphatic tissues and by tumors from ribose-C14. The same tissues formed labeled serine from formate-C14 and glycine.
* Aided in part by grants from the National Cancer Institute, Department of Health, Education and Welfare, and by the American Cancer Society. The author is indebted to Odette Graham, with whose assistance the experiments described below were performed.
Received 6/21/55.
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