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Enzymatic Deamination of 8-Azaguanine in Normal Human Brain and in Glioblastoma Multiforme^*

Erich Hirschberg, Margaret R. Murray, Edith R. Peterson, Jacob Kream, Raoul Schafranek and J. Lawrence Pool

( Institute of Cancer Research and Departments of Biochemistry, Medicine, Surgery, and Neurological Surgery, Columbia University, College of Physicians and Surgeons, New York 32, N.Y.)

1. The human brain tumor, glioblastoma multiforme, when grown in tissue culture, is severely damaged by exposure to 8-azaguanine.

2. Fetal human brain, the only available nonneoplastic control for tissue culture experiments, is less severely damaged by exposure to this agent and recovers more rapidly and more completely when the agent is removed.

3. 8-Azaxanthine, the end product of the enzymatic deamination of 8-azaguanine, causes no damage of any kind to either of these tissues in tissue culture.

4. Homogenates of glioblastoma are devoid of measurable a zaguanine deaminase activity; homogenates of non-neoplastic adult brain exhibit the highest deaminase activity of any animal tissue which has been studied.

5. Chromatographic analysis of feeding fluids after incubation with glioblastoma explants in tissue culture confirms the virtual absence of azaguanine deaminase activity from the cells of this tissue. Fetal brain is somewhat better able to carry out the deamination of this agent, but even this slightly greater deaminase activity is very small when compared to the activity of adult human brain.

^* This investigation was supported in part by a research grant (C-1386) from the National Cancer Institute, of the National Institutes of Health, Public Health Service, and in part by the John Gunther, Jr., Memorial Fund.

Present address: Basic Research Laboratory, Veterans Administration Hospital, Brooklyn, N.Y.

Received 10/ 6/52.