96
RATE OF REPAIR OF RADIATION DAMAGE IN MICE
THE SHORTER-TERM BIOLOGICAL HAZARDS OF A FALLOUT FIELD
100,
t
‘
T
t
half-times for repair of the fast component were
T
140
T
T
Py
rery
T
T
TET
TTT
T
T
wT
Trey
97
T
remy
ere
1.2, 2.0, and 2.4 hours, respectively, for initial
doses of 400, 600, and 800 r.
On the basis of the preceding results, the
following tentative conclusions were reached:
1. The damage leading to death in the
first 100 hours repairs at a faster rate
than the damage responsible for 30-day
lethality.
2. Repair in both cases appears to consist
of two components, one component having a short half-time and the other a
T= 33 OAYS
long half time.
3. Neither the extent of percent residual
T
RESIDUAL DAMAGE (% OF INITIAL}
50]
damage nor the repair half-time is affected by the size of the initial dose in
2or-
4
& 100;-
7
3
<
=
w
4s
°o
se 80}-
=o
>
a
~~.
te
™~
~~
s
~~
° a
> 60;--
oO
4
~~
m™~
=
~|
_!
<q
B 40h
100
T
T
t
T
T
oa
T
w
20/1600
2000
3060
TIME BETWEEN DOSES (HOURS)
Ficure 2.—Slow component in repair of damage contributing te 80-day lethality.
by the inverse of the variance and the com-
mon slope obtained. These data are plotted
in Figure 5. It is thought that this plot represents the slow component of repair. The halftime was approximately 15 days as opposed to
the half-time of 33 days obtained when the
LD,-30 days was used as the end-point. By
subtracting the contribution of the slow component from thetotal effect, it was possible to
obtain values for the fast component.
percent total residual at time 0 and probably
The
8-hour values fell badly out of line and ac-
cordingly were not used in this figure.
oe
sor-
4
The
0
0
po
i
05
1
pe
5
10
td
50
too
pe
:
§00 1000
TIME BETWEEN DOSES (HOURS)
the case of 30-daylethality.
30]
20;-
°
Ty19-10 HRS,
2
Both the
extent of percent residual and the repair
rate of the fast component are propor-
tional to dose in the case of 100-hour
death.
4. No evidence of a permanent level of
residual damage was obtained in either
study.
5. Since repair of damage leading to death
by two different mechanisms showsdifa
et
Frioure 4.—Perceni residual damage as mcasured by depressionof the LDgy-100 hours as a function of log time.
40)
These
data are shown in Figure 6. The regression
lines shown were arbitrarily forced through the
zero time point since this point is based on 100
has more validity than the other points.
OO GOOr INITIAL DOSE
a— ai BOOr INITIAL DOSE
RESIDUAL INJURY {% OF INITIAL)
‘
4
o———@ 400r INITIAL DOSE
1
4
!
|
J
wt.
|
6
12
16
20
24
TIME BETWEEN DOSES (HOURS)
Figure 3.-~Fast component in repair of damage contributing to 30-day lethality.
ferent characteristics, it is likely that
death from other mechanisms (such as
premature aging) will also differ from
the two mechanisms studied.
6. The residual injury leading to life shortening is probably not related to the
residual injury measured in the present
studies, since it is reasonably certain
that a permanentresidual injury causcs
life shortening. No permanent residual
was detected in these studies.
7. Both the LDy-30 days and the LDy»-
100 hours should be dose rate dependent
with
more
very
fast
the LD»-100 hours being much
rate dependent because of the
short half-time for repair of the
component. Preliminary studies
have supported this view.