Metabolic Processes Involved in the Development of Nuclear Pyknosis in Irradiated Rat Thymocytes

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Abstract
The development of nuclear pyknosis in x-irradiated rat thymocytes has been shown to be closely correlated with the intracellular labilization of DNA from their nucleoprotein. The development of pyknosis is completely dependent on the respiratory activity of the cell. It is prevented or slowed by any metabolic inhibitor which retards the respiration of the cell. It is not dependent on the level of ATP within the cell and can be prevented by inhibitors which produce a high intracellular level of inorganic phosphate. The development of nuclear pyknosis can, however, be accelerated by high concentrations of phosphate and by serum. Intracellular phosphate facilitates the dissociation of DNA from the damaged nucleoprotein. There is no evidence for increased levels of inorganic phosphate or phosphate uptake, by irradiated cells. There is evidence for damage to the respiratory mechanism of the irradiated cell. Large thymocytes which label with 3H-TdR are more resistant to irradiation than are the smaller unlabelled cells. Regenerating, newly-formed thymocytes are more sensitive to irradiation than the normal equilibrium population of the thymus.

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