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Amino Acid Induction and Carbohydrate Repression of Dimethylnitrosamine Demethylase in Rat Liver¹

Seamen's Memorial Research Laboratory, USPHS Hospital, New Orleans, Louisiana 70118, and Department of Medicine (Biochemistry), Tulane University School of Medicine, New Orleans, Louisiana 70112

Starvation of rats for 24 hr considerably enhances hepatic dimethylnitrosamine demethylase activity, and 3-methylcholanthrene pretreatment inhibits the enzyme in starved animals to the same extent as in fed animals. Determination of the kinetic constants following starvation revealed significant increase of the apparent V_max indicating increase in the amount of demethylase. There was no significant change in the K_m. Studies with actinomycin D provide strong support that starvation-induced increase is due to de novo protein synthesis, consistent with the observed increase in maximal velocity.

Ingestion of glucose markedly inhibits demethylase activity while ingestion of casein alone stimulates it appreciably, in a manner analogous to such phenomena with a few other hepatic enzymes. These results and previous data suggest that the level of dimethylnitrosamine demethylase in liver is under the control of multiple regulatory factors.

¹ This investigation was supported by the USPHS Research Grant CA-05793 from the National Cancer Institute and by a Grant-in-Aid from the Greater New Orleans Cancer Association, Inc. Presented in part at the Tenth International Cancer Congress, Houston, Texas, May 1970. Abstract No. 15.

Received 4/ 9/70. Accepted 7/ 1/70.