The precise mechanism by which Hydroxyurea produces its cytotoxic effects cannot, at present, be described. However, the reports of various studies in tissue culture in rats and man lend support to the hypothesis that Hydroxyurea causes an immediate inhibition of DNA synthesis without interfering with the synthesis of ribonucleic acid or of protein. This hypothesis explains why, under certain conditions, it may induce teratogenic effects. Three mechanisms of action have been postulated for the increased effectiveness of concomitant use of Hydroxyurea therapy with irradiation on squamous cell (epidermoid) carcinomas of the head and neck. In vitro studies utilizing Chinese hamster cells suggest that Hydroxyurea is lethal to normally radioresistant S – stage cells, and holds other cells of the cell cycle in the G-1 or pre-DNA synthesis stage where they are most susceptible to the effects of irradiation. The third mechanism of action has been theorized on the basis of in vitro studies of HeLa cells; it appears that Hydroxyurea, by inhibition of DNA synthesis, hinders the normal repair process of cells damaged but not killed by irradiation, thereby decreasing their survival rate; RNA and protein synthesis have shown no alteration.