These slopes plotted on a semilogarithmic scale as a function of the exposure
rate (R/day) gave in turn straight relations thus justifying the conclusion
that the slope of the Gompertz lines increased exponentially with daily dose
(see Figure VII B).
Finally, this paper [S5| has interesting aspects con-
cerning the cellular mechanisms of life-shortening because it provides some
link between phenomena at the whole-body level and at the cell population level.
12e.
The paper by Grahn, Fry and Lea [G5] summarized a number of studies on
various strains of young adult mice exposed to various levels of 600, gamma—
radiation ranging from 0.3 to over 30 R/day and discussed the problem of a
"non-specific" life-shortening effect as opposed to a "specific" effect, that
is the induction of neoplasia.
Data from mouse strains Balb/c, C57BL/6 and
their F, hybrid show upon irradiation a steady increment of mortality associa-
ted with neoplastic disease as both the age and the daily dosage increase up
to a few R/day.
An excess mortality from non-neoplastic conditions with re-
spect to controls is seen only at 6 R/day and above.
Thus, the risk of early
or excess death from radiation exposure at intensities of the order of 100 or
200 times the background would be related entirely to the increase in inci-
dence and to the shift in the time of appearance of the neoplastic diseases.
123.
Sacher [S14] pointed out that when the slope of the Gompertz curves ob-
tained at various daily doses is plotted as a function of the daily dose on a
double logarithmic scale for two mouse strains, the LAF1
[S4] and BCF1
[$5]
the resulting relationship can be resolved into two straight branches (see
Figure VIII).
At exposure rates below 24 R/day the data lie close to a first-
power line while above this value they conform closely to a second-power
trend.
At about 2h R/day the contribution of the two terms is equal.
These
observations would be consistent with the hypothesis that life-shortening at
dose rates in excess of the above-cited value is predominantly due to a type
of cytogenetic injury viewed as lethal rearrangements following chromosome
breakage (dicentries).
On the contrary, at lower dose rates one-event lethal
aberrations (terminal deletions, dominant point-mutations) would predominantly
or exlcusively be involved.
gle event kinetics.
Life-shortening by fast neutrons would obey sin-