Is the NAD-poly (ADP-ribose) Polymerase System the Trigger in Radiation-induced Death of Mouse Thymocytes?

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Abstract
Agents that induce DNA strand breaks evoke a drop in the NAD content in mouse thymocytes. A decrease in the endogenous NAD content that occurs immediately after γ-irradiation of thymocytes is entirely attributed to the activation of poly(ADP-ribosylation). The addition of 5 mm benzamide before irradiation prevents the postirradiation drop of the NAD level but has no effect on chromatin degradation and cell death. In contrast to liver nuclei, preincubation of mouse thymic nuclei with NAD had no effect on the subsequent chromatin endonucleolysis by Ca2+/Mg2+-dependent endonuclease. It is suggested that the NAD-poly(ADP-ribose) polymerase system is probably not the trigger in the radiation-induced programmed death of mouse thymocytes, but may merely be indicative of the radiation response of these cells.

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