Radionuclide Toxicity in Cultured Mammalian Cells: Elucidation of the Primary Site for Radiation-Induced Division Delay

In Vivo Therapy of Neoplastic Meningitis with Methotrexate and 5-[125I]iodo-2'-deoxyuridine

“…Because of its predominant IC decay (93%) following EC, this radionuclide is a proli® c emitter of Auger electrons (mean of 21 per decay (25) IUdR leads to (i) the production of \ 1 DNA double-strand break (26) and (ii) an exponential reduction in cell survival (22, 27± 32) with a high relative biologic effectiveness value of 7.2 (22,33,34). In contrast, the decay of this radionuclide within the cell cytoplasm (13,35), af® xed to cell plasma membranes (35), or extracellularly (22,23) produces no extraordinary lethal effects with survival curves (i) resembling those observed with x-ray (having a distinct shoulder in murine cells) and (ii) exhibiting shallower slopes.…”

Induction of apoptosis in human tumor cells after exposure to Auger electrons: comparison with γ-ray exposure

“…The highly localized nature of energy absorption leads to severe damage of molecular structures only in the immediate vicinity of the decaying atom [27][28][29][30]. In vitro studies at the molecular and cellular levels have repeatedly demonstrated (i) the very high toxicity and efficient double-strand-break (DSB) formation when such radionuclides decay in close proximity to nuclear DNA [24,[31][32][33][34], and (ii) the relative ineffectiveness of these radionuclides when the decay occurs in the cytoplasm or outside the cell [25,35,36]. In comparison, γ -radiation is much less efficient in DSB formation and produces reactive oxidative species (ROS) throughout the irradiated cell, i.e.…”

The Effect of Fractionated Irradiation on Cell Kinetics

“…3). The irradiation-induced G2/M delays were 2.2 h, 3.5 h, 5.5 h, and 7.5 h for doses of 1 Gy, 2 Gy, 3 Gy, and 6 Gy respectively.…”

“…Cells are susceptible to x-ray-induced G2 delay through most of the cell cycle (I). The target for the G2 block is located in or near the nucleus (7) or possibly in a structure associated with DNA (8). The delay in progression of cells in the cycle is not necessarily caused by the DNA damage per se (9).…”