lithium-chloride and Carcinoma--Ehrlich-Tumor

The activity of spermidine/spermine N1-acetyltransferase (SAT) was enhanced in Ehrlich ascites tumor cells by the addition of lithium chloride. Na+ did not affect the enzyme activity. Total RNA was isolated from cells treated with LiCl and the relative abundance of the SAT mRNA was measured by Northern blot analysis. The levels in cells treated with LiCl were comparable to those in control cells. In the treated cells, the biological half-life of SAT was approximately 20 min, which was the same as for control cells. When LiCl and H-7, a protein kinase inhibitor, were added simultaneously to culture, the elevation caused by LiCl of SAT activity was reduced. LiCl did not cause maximum enhancement of the enzyme in cells treated beforehand with a higher concentration of TPA. These results suggest that treatment of Ehrlich ascites tumor cells with LiCl enhanced SAT activity during translation, not during transcription or after translation and that the enhancement of SAT by LiCl is probably mediated by protein kinase C.

Topics: 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine; Acetyltransferases; Animals; Blotting, Northern; Carcinoma, Ehrlich Tumor; Chlorides; Enzyme Induction; Isoquinolines; Lithium; Lithium Chloride; Piperazines; Protein Kinase Inhibitors; RNA, Messenger; Tetradecanoylphorbol Acetate; Tumor Cells, Cultured

The activity of ornithine decarboxylase (ODC) was increased in Ehrlich ascites tumor cells by a change of the medium. This increase in the activity was inhibited by the addition of LiCl to the medium. Na+ and Mg2+ did not affect the enzyme activity. The inhibition of the enzyme activity with LiCl was not reversed by the addition of inositol or dibutyryl cyclic AMP. Total RNA was isolated from cells treated with LiCl and the relative abundance of the ODC mRNA was measured by Northern blot analysis. These levels in cells treated with LiCl were comparable to those in control cells. In the treated cells, the biological half-life of ODC was 14 min, which was the same as for the control cells. The inhibition by LiCl of ODC activity was not due to the nonspecific toxicity of LiCl. These results suggest that treatment of Ehrlich ascites tumor cells with LiCl suppressed ODC induction during translation, not during transcription or after translation.

Topics: Animals; Carcinoma, Ehrlich Tumor; Chlorides; Dose-Response Relationship, Drug; Enzyme Induction; Gene Expression Regulation, Enzymologic; Lithium; Lithium Chloride; Ornithine Decarboxylase; RNA, Messenger; Tetradecanoylphorbol Acetate; Tumor Cells, Cultured