In the RPMI mouse renal cell tumor, N1-acetylspermidine (N1AS) was found to be constant and major component (18 to 25%) of the polyamine pool. Early i.m. growth induced urinary N1AS excretions up to tenfold normal, equivalent to a daily turnover of the entire tumor polyamine pool. N1AS excretion was correspondingly lower during more limited s.c. tumor growth. In nine other mouse tumors, N1AS pools were low or negligible, and correspondingly urinary N1AS or N8AS increased only in advanced growth, and less significantly. Urinary N1AS was elevated likewise in immature untumored mice. Thus, the enriched N1AS pool of the renal cell tumor was separately distinguishable as a direct source of elevation of urinary N1AS. N1AS was selectively abolished from the renal cell tumor by prolonged BCNU treatment, but was not rapidly depleted by the polyamine inhibitor DFMO. In cell culture, the RPMI renal cell tumor contained unusually high uninduced levels of sperm(id)ine N1-acetyltransferase, a potential source of N1AS. N1AS pools were also significantly elevated in human renal cell tumors.
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