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1,2-Dimethylhydrazine-induced Alterations in N¹-Acetylspermidine Levels and Spermidine N¹-Acetyltransferase Activity in Rat Colonic Mucosa¹

Departments of Medicine, The University of Chicago and Michael Reese Hospitals, Pritzker School of Medicine of The University of Chicago, Chicago, Illinois 60637

To determine whether alterations in the "reverse" or "conversion" pathway for putrescine formation were involved in the induction of colonic tumors by 1,2-dimethylhydrazine, male albino rats of the Sherman strain were given injections s.c. of this agent (20 mg/kg body weight/week) or diluent for 5, 10, 15, and/or 26 weeks. Animals were sacrificed at each of these time periods and polyamine levels, including N¹- and N⁸-acetylspermidine, as well as the activities of ornithine decarboxylase, spermidine N¹-acetyltransferase and polyamine oxidase were measured and compared in rat proximal and distal colonic mucosa of each group.

The results of these studies demonstrated that: (a) N¹- and N⁸-acetylspermidine levels were similar in the control and treated proximal colonic segments at all time periods examined; (b) N¹- and N⁸-acetylspermidine levels were also similar in the control and treated distal colonic segments at 5 and 10 weeks; (c) at 15 weeks the level of N¹-acetylspermidine, but not N⁸-acetylspermidine, however, was increased in the treated distal colonic segment secondary to increases in the activity of spermidine N¹-acetyltransferase; and (d) at 26 weeks, the level of N¹-acetylspermidine remained higher in treated distal "uninvolved" colonic tissue and were markedly elevated in colonic tumors in both segments. Based on these findings, it would appear that the reverse pathway for putrescine formation may be involved in the 1,2-dimethylhydrazine-induced malignant transformation process of the rat colon.

¹ Supported by USPHS Grants CA 36745 and CA 08266 awarded by the National Cancer Institute, Department of Health and Human Services.

² Recipient of a Merit Award from the National Cancer Institute, NIH. To whom requests for reprints should be addressed, at The University of Chicago Hospitals and Clinics, Box 400, Chicago, IL 60637.

Received 5/31/88. Revised 10/ 3/88. Accepted 10/24/88.