Nicotinamide (NA), a naturally occuring vitamin and a protease inhibitor, has been shown to be effective in treating some skin ailments. It inhibits cell proliferation and induces cell differentiation. This report shows the effects of NA on mouse skin tumor development and on the critical events involved in this process. NA reduced tumor growth, inhibited the 12-O-tetradecanoylphorbol- 13-acetate (TPA) induced ornithine decarboxylase activity, but induced the transglutaminase activity which was inhibited by TPA under different experimental conditions.The effects of NA on ornithine decarboxylase (ODC) and transglutaminase (TG) indicated that nicotinamide (NA) probably programmmed the cells for their death in the natural course of time, I.e. Programed cell death. This observation indicates that NA might be a better agent for the detailed study and for the better use in prevention of cancer alone or in combination with other drugs.

Nicotinamide (NA), a relatively nontoxic compound, has been shown to inhibit tumor development, induce differentiation, increase the sensitization of the anticancer drug resistant cancer cells and is being used in different skin ailments. But there are not many reports on its mechanism of action. Here we report that NA induced endonuclease activity. This endonuclease induction by NA appeared to be dose dependent and a function of time. As evident by the use of modifiers of DNase I, this endonuclease appeared to be like DNase type I. Increased [3H] thymidine incorporation in DNA in the presence of NA is possibly a consequence of increased 3-OH'nicks due to increased DNA fragmentation by increased endonuclease activity. The present results would be of help in the better understanding of the mechanism of NA action and its improved use in cancer control.