The relationship of lysosomal stability to radiation-induced delay of cell division in Tetrahymena pyriformis Public Deposited

http://ir.library.oregonstate.edu/concern/graduate_thesis_or_dissertations/st74cs94n

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  • Cell division in a heat synchronized Tetrahymena pyriformis (GL-I) cell can be delayed if the cell is exposed to X-irradiation (300 kVp, 20 mA, HVL = 0. 9 mm Cu, 25 R/ sec) prior to a critical time after the end of the synchronizing treatment (EST). At the critical time, the cells undergo a rapid transition from a state of being sensitive to being delayed to one of relative insensitivity. After this time, the coming division is delayed little if at all; that is, there is an "all or none" transition to insensitivity to division delay. However, the second division is delayed, indicating that damage has occurred. The transition point (median critical time) is determined by interpolating the time after EST at which a given radiation exposure splits a population of cells into 50 percent delayed and 50 percent not delayed. The transition point is dose dependent in that the larger the exposure, the later the transition point (31 minutes after EST for 3kR increasing gradually to 51 minutes after EST for 18.5 kR). The division delay response is correlated with a resorption of the developing new mouth as determined from silver stained cells fixed every ten minutes after EST. The length of time for the oral primordium to be resorbed increases as the dose increases and varies with the time of irradiation relative to the transition point. The all or none" nature of the division delay response and the fact that cells irradiated after the transition point seemingly "ignore" the radiation damage until the second generation, together suggest that the damage produced by the irradiation may or may .not trigger a cellular response that results in cell division delay and oral primordium resorption. These responses might suggest that preformed enzymes, possibly from lysosomes, could be involved. Therefore, cells were treated with a known lysosomal stabilizer (hydrocortisone) and a labilizer (vitamin A) continuously before, during, and after exposure to 7.5 kR of X-rays. Cells treated with hydrocortisone- 21- phosphate (5.0 mM) showed an earlier transition point (36.5 minutes after EST) whereas cells treated with vitamin A-acetate (0.2 mM) showed a later transition point (50.5 minutes after EST) relative to the transition point for untreated, irradiated cells (43 minutes after EST). The time of the transition for cells treated with a lysosomal stabilizer (depresses enzyme release) and 7.5 kR corresponds to the transition point for untreated cells irradiated with only 5.0 kR,suggesting less sensitivity. Conversely, the transition point for cells treated with a lysosomal labilizer (enhances enzyme release) and 7.5 kR corresponds to the time of transition for untreated cells exposed to 18.5 kR, suggesting greater sensitivity. However, in all cases, 7.5 kR delayed the divisions about the same amount, whether the agents were present or not, indicating that the agents do not act in a simple dose - modifying manner. The data are consistent with the hypothesis that irradiation produces damage that may or may .not trigger off a cellular response that leads to delay of division. The sensitivity of the cell to being triggered to delay division may involve lysosomes.
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