A study of the rates of incorporation of3 H-thymidine (<tex-math>${}^{3}{\rm HTdR}$</tex-math>) and <tex-math>${}^{3}{\rm H}\text{-deoxycytydine}$</tex-math> (<tex-math>${}^{3}{\rm HCdR}$</tex-math>) into the DNA of human lymphocytes following exposure to ionizing radiation suggests the presence of two processes: One is rapid, essentially completed within an hour after irradiation; the other is slow and persists for at least 7 hours after irradiation. The rapid process can be adequately represented by a simple enzyme model for which the substrates are <tex-math>${}^{3}{\rm HTdR}$</tex-math> or <tex-math>${}^{3}{\rm HCdR}$</tex-math> and the radiation-induced lesions in the DNA. In terms of the model, the effect of anoxia is to decrease two-fold the concentration of lesions. The action of phytohemagglutinin is to double the concentration of enzyme prior to the onset of normal DNA synthesis. The slow process can also be represented by a simple enzyme model with radiation-induced lesions as substrate.

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