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016 - Effects on Mammals · Percheron horse

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  Speaker 1: Section fifteen of the Genetic Effects of radiation. This is
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  Speaker 1: a LibriVox recording. All LibriVox recordings are in the public domain.
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  Speaker 1: For more information or to volunteer, please visit LibriVox dot org.
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  Speaker 1: Read by T. R. Love of Pleasant Hill, California. The
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  Speaker 1: Genetic Effects of Radiation by Isaac Asimov and Theodosius Dovzansky,
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  Speaker 1: Section fifteen effects on mammals. Although genetic findings on such
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  Speaker 1: comparatively simple creatures as fruit flies and bacteria seem to
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  Speaker 1: apply generally to all forms of life, it seems unsafe
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  Speaker 1: to rely on these findings completely in anything as important
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  Speaker 1: as possible genetic damage to man through radiation. During the
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  Speaker 1: nineteen fifties and nineteen sixties, therefore, there have been important
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  Speaker 1: studies on mice, particularly by w. U. L. Russell at
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  Speaker 1: Oakridge National Laboratory, Oakridge, Tennessee. While not as short lived
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  Speaker 1: or as secined as fruit flies, mice can nevertheless produce
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  Speaker 1: enough young over a reasonable period of time to yield
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  Speaker 1: statistically useful results. Experimenters have worked with hundreds of thousands
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  Speaker 1: of offspring born of mice that have been irradiated with
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  Speaker 1: gamma rays and X rays in different amounts and at
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  Speaker 1: different intensities, as well as with additional hundreds of thousands
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  Speaker 1: born to mice that were not irradiated. Since mice, like men,
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  Speaker 1: are mammals, results gained by such experiments are particularly significant.
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  Speaker 1: Mice are far closer to man in the scheme of
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  Speaker 1: life than is any other creature that has been studied
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  Speaker 1: genetically on a large scale, and their reactions, one might
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  Speaker 1: cautiously assume, are likely to be closer to those that
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  Speaker 1: would be found in man. Almost at once when the
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  Speaker 1: studies began, it turned out that mice were more susceptible
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  Speaker 1: to genetic damage than fruitflies were. The induced mutation rate
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  Speaker 1: per gene seems to be about fifteen times that found
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  Speaker 1: in Drosophila for comparable X ray dosis. The only safe
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  Speaker 1: course for mankind, then is to air, if it must
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  Speaker 1: strongly on the side of conservatism. Once we have decided
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  Speaker 1: what might be safe on the basis of Drosophilus studies,
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  Speaker 1: we ought then to tighten precautions several notches by remembering
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  Speaker 1: that we are very likely more vulnerable than fruitflies are counteracting.
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  Speaker 1: The depressing nature of this finding was that of a
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  Speaker 1: later quite unexpected discovery. It was well established that in
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  Speaker 1: fruitflies and other simple organisms, it was the total dosage
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  Speaker 1: of absorbed radiation that counted, and that whether this was
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  Speaker 1: delivered quickly or slowly did not matter. This proved to
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  Speaker 1: be not so in the case of mice. In male mice,
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  Speaker 1: a radiation dose delivered at the rate of zero point
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  Speaker 1: zero zero nine rad per minute produced only from one
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  Speaker 1: quarter to one third as many mutations as did the
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  Speaker 1: same total dose delivered at ninety rads per minute. In
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  Speaker 1: the male cells in the gonads are constantly dividing to
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  Speaker 1: produce sex cells, the latter are produced by the billions.
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  Speaker 1: It might be then, that at low radiation dose rates,
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  Speaker 1: a few of the gonad cells are damaged, but that
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  Speaker 1: the undamaged ones produce a flood of sperm cells, drowning
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  Speaker 1: out the few produced by the damaged gonad cells. The
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  Speaker 1: same radiation dose delivered in a short time might, however,
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  Speaker 1: damage so many of the gonad cells as to make
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  Speaker 1: the damaged sex cells much more difficult to flood out.
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  Speaker 1: A second possible explanation is that there is present within
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  Speaker 1: the cells themselves, some process that tends to repair damage
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  Speaker 1: to the cells and to counteract mutations. It might be
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  Speaker 1: a slow working, laborious process that could keep up with
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  Speaker 1: the damage inflicted at load dosage rates, but not at
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  Speaker 1: high ones. High dosage rates might even damage the repair
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  Speaker 1: mechanism itself. That too, would account for the fewer mutations
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  Speaker 1: at load dosage rates than at high ones. To check
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  Speaker 1: which of the two possible explanations was nearer the truth,
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  Speaker 1: Russell performed similar tests on female mice. In the female mouse,
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  Speaker 1: or the female human being for that matter, the egg
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  Speaker 1: cells have completed almost all their divisions before the female
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  Speaker 1: is born. There are only so many cells in the
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  Speaker 1: female gonants that can give rise to egg cells, and
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  Speaker 1: each one give rise to only a single egg cell.
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  Speaker 1: There is no possibility of damaged egg cells being drowned
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  Speaker 1: out by floods of undamaged ones, because there are no floods. Yet.
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  Speaker 1: It was found that in the female mouse the mutation
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  Speaker 1: rate also dropped when the radiation dose rate was decreased.
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  Speaker 1: In fact, it dropped even more drastically than was the
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  Speaker 1: case in the male mouse. Apparently, then there must be
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  Speaker 1: actual repair within the cell. There must be some chemical
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  Speaker 1: mechanism inside the cell capable of counteracting radiation damage to
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  Speaker 1: some extent. In the female mouse, the mutation rate drops
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  Speaker 1: very low as the radiation dose rate drops, so that
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  Speaker 1: it would seem that almost all mutations might be repaired
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  Speaker 1: given enough time. In the male, the mutation rate drops
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  Speaker 1: only so far and no farther, so that some mutations
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  Speaker 1: about one third is the best estimate so far, cannot
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  Speaker 1: be repaired. If this is also true in the human being,
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  Speaker 1: and it is at least reasonably likely that it is,
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  Speaker 1: then the greater vulnerability of our genes as compared with
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  Speaker 1: those of fruitflies, is at least partially made up for
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  Speaker 1: by our greater ability to repair the damage. This opens
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  Speaker 1: a door for the future too. The workings of the
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  Speaker 1: gene repair mechanism ought it is to be hoped eventually
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  Speaker 1: to be puzzled out. When it is, methods may be
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  Speaker 1: discovered for reinforcing that mechanism, speeding it and increasing its effectiveness.
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  Speaker 1: We may then find ourselves no longer completely helpless in
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  Speaker 1: the face of genetic damage or even of radiation sickness.
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  Speaker 1: On the other hand, it is only fair to point
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  Speaker 1: out that the foregoing appraisal may be an over optimistic
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  Speaker 1: Viewmussel's experiments involve just seven genes, and it is possible
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  Speaker 1: that these are not representative of the thousands that exist altogether.
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  Speaker 1: While the work done so far is most suggestive and interesting,
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  Speaker 1: much research remains to be carried out. If then we
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  Speaker 1: cannot help hoping that natural devices for counteracting radiation damage
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  Speaker 1: may be developed in the future, we must for the
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  Speaker 1: present remain rigidly cautious. End of Section fifteen.