Although genetic findings on such comparatively simple creatures as
fruit flies and bacteria seem to apply generally to all forms of life,
it seems unsafe to rely on these findings completely in anything as
important as possible genetic damage to man through radiation. During
the 1950s and 1960s, therefore, there have been important studies on
mice, particularly by W. L. Russell at Oak Ridge National Laboratory,
Oak Ridge, Tennessee.
While not as short-lived or as fecund as fruit flies, mice can
nevertheless produce enough young over a reasonable period of time to
yield statistically useful results. Experimenters have worked with
hundreds of thousands of offspring born of mice that have been
irradiated with gamma rays and X rays in different amounts and at
different intensities, as well as with additional hundreds of thousands
born to mice that were not irradiated.
Since mice, like men, are mammals, results gained by such experiments
are particularly significant. Mice are far closer to man in the scheme
of life than is any other creature that has been studied genetically on
a large scale, and their reactions (one might cautiously assume) are
likely to be closer to those that would be found in man.
Almost at once, when the studies began, it turned out that mice were
more susceptible to genetic damage than fruit flies were. The induced
mutation rate per gene seems to be about fifteen times that found in
_Drosophila_ for comparable X ray doses. The only safe course for
mankind then is to err, if it must, strongly on the side of
conservatism. Once we have decided what might be safe on the basis of
_Drosophila_ studies, we ought then to tighten precautions several
notches by remembering that we are very likely more vulnerable than
fruit flies are.
Counteracting the depressing nature of this finding was that of a later,
quite unexpected discovery. It was well established that in fruit flies
and other simple organisms, it was the total dosage of absorbed
radiation that counted and that whether this was delivered quickly or
slowly did not matter.
[Illustration: _Arrangement for long-term low-dose-rate irradiation of
mice used for mutation-rate studies at Oak Ridge National Laboratory.
The cages are arranged at equal distances from a cesium-137 gamma-ray
source in the lead pot on the floor. The horizontal rod rotates the
source._]
This proved to be _not_ so in the case of mice. In male mice, a
radiation dose delivered at the rate of 0.009 rad per minute produced
only from one-quarter to one-third as many mutations as did the same
total dose delivered at 90 rads per minute.
In the male, cells in the gonads are constantly dividing to produce sex
cells. The latter are produced by the billions. It might be, then, that
at low radiation dose rates, a few of the gonad cells are damaged but
that the undamaged ones produce a flood of sperm cells, “drowning out”
the few produced by the damaged gonad cells. The same radiation dose
delivered in a short time might, however, damage so many of the gonad
cells as to make the damaged sex cells much more difficult to “flood
out”.
A second possible explanation is that there is present within the cells
themselves some process that tends to repair damage to the genes and to
counteract mutations. It might be a slow-working, laborious process that
could keep up with the damage inflicted at low dosage rates but not at
high ones. High dosage rates might even damage the repair mechanism
itself. That, too, would account for the fewer mutations at low dosage
rates than at high ones.
To check which of the two possible explanations was nearer the truth,
Russell performed similar tests on female mice. In the female mouse (or
the female human being, for that matter) the egg cells have completed
almost all their divisions before the female is born. There are only so
many cells in the female gonads that can give rise to egg cells, and
each one gives rise to only a single egg cell. There is no possibility
of damaged egg cells being drowned out by floods of undamaged ones
because there are no floods.
Yet it was found that in the female mouse the mutation rate also dropped
when the radiation dose rate was decreased. In fact, it dropped even
more drastically than was the case in the male mouse.
Apparently, then, there must be actual repair within the cell. There
must be some chemical mechanism inside the cell capable of counteracting
radiation damage to some extent. In the female mouse, the mutation rate
drops very low as the radiation dose rate drops, so that it would seem
that almost all mutations might be repaired, given enough time. In the
male, the mutation rate drops only so far and no farther, so that some
mutations (about one-third is the best estimate so far) cannot be
repaired.
If this is also true in the human being (and it is at least reasonably
likely that it is), then the greater vulnerability of our genes as
compared with those of fruit flies is at least partially made up for by
our greater ability to repair the damage.
This opens a door for the future, too. The workings of the gene-repair
mechanism ought (it is to be hoped) eventually to be puzzled out. When
it is, methods may be discovered for reinforcing that mechanism,
speeding it, and increasing its effectiveness. We may then find
ourselves no longer completely helpless in the face of genetic damage,
or even of radiation sickness.
On the other hand, it is only fair to point out that the foregoing
appraisal may be an over-optimistic view. Russell’s experiments involved
just 7 genes and it is possible that these are not representative of the
thousands that exist altogether. While the work done so far is most
suggestive and interesting, much research remains to be carried out.
If, then, we cannot help hoping that natural devices for counteracting
radiation damage may be developed in the future, we must, for the
present, remain rigidly cautious.