This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Clark, B. R. Articles by Smith, R. A. Search for Related Content PubMed PubMed Citation Articles by Clark, B. R. Articles by Smith, R. A.

Altered Distribution and Excretion of N¹-Methylnicotinamide in Rats with Walker 256 Carcinosarcoma¹

Departments of Chemistry [B. R. C., J. T. M., A. P., P. A. M., and R. A. S.] and Medicine [R. M. H.], and the Molecular Biology Institute, University of California, Los Angeles, California 90024

Levels of nicotinamide and N¹-methylnicotinamide in serum, liver, and kidney as well as renal clearances and 24-hr urine levels of N¹-methylnicotinamide were compared in normal rats and rats bearing Walker 256 tumors. There was no significant difference between normal and tumor-bearing rats with regard to nicotinamide levels. With regard to N¹-methylnicotinamide, tumor-bearing rats had significantly lower serum and liver levels and significantly higher 24-hr urine levels and renal clearances.

Walker 256 tumor tissue and liver and kidney from a normal and a tumor-bearing rat were separately examined for S-adenosylmethionine:nicotinamide methyltransferase activity. The specific activity in tumor tissue extract was greater than that in each liver extract, which, in turn, was much greater than the specific activity in each kidney extract. However, the specific activity in each tissue (liver and kidney) from the tumor-bearing rat was equal to the specific activity in the corresponding tissue of the normal rat.

S-Adenosylmethionine:nicotinamide methyltransferase was obtained with 18-fold purification from a tissue extract of Walker 256 tumor. The enzyme activity required activation by thiols, and maximal activity was observed at pH 8.6. The K_m's for the substrates, S-adenosylmethionine and nicotinamide, were 7.0 x 10^-3 mM and 0.50 mM, respectively. The K_i's for the products, S-adenosylhomocysteine and N¹-methylnicotinamide, were, respectively, 25 x 10^-3 mM and greater than 5 mM.

¹ This research was supported by USPHS Grant 5 T01 GM 00463-13, the Julius and Dorothy Fried Foundation and Grant CA 13196. Chemistry Department Publication No. 3374.

² Present address: B-4 Neurology, Harbor General Hospital, Torrance, Calif. 90509.

Received 8/15/74. Accepted 3/25/75.

This article has been cited by other articles:

				F. Kull Jr, D. Brent, I Parikh, and P Cuatrecasas Chemical identification of a tumor-derived angiogenic factor Science, May 15, 1987; 236(4803): 843 - 845. [Abstract] [PDF]