|Abstract or Summary
- 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.