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PubMed1976

Evaluation and re-evaluation of genetic radiation hazards in man. III. Other relevant data and risk assessment.

Some of the advances in mammalian radiation genetics, human genetics and cytogenetics that were made during the last 2-3 years and that have either a direct bearing on, or that may be potentially useful in, the evaluation of genetic radiation hazards in man have been examined. Among these are (1) the new data on the incidence of genetic diseases in man; (2) the latest results of the study of mortality rates among children born to survivors of the atomic bombings of Hiroshima and Nagasaki; (3) new data on the radiation-induction of reciprocal translocations in human spermatogonia; (4) new results from radiation studies with mice on skeletal mutations, autosomal recessive lethals, sex-chromosome losses, translocation induction and recovery etc., and (5) a re-analysis of the earlier data on dose-rate effects for the induction of specific locus mutations in mouse spermatogonia. Using the pertinent new information as a basis, quantitative estimates are presented employing both a direct method of expressing risks in terms of effects per unit dose of irradiation and the indirect doubling-dose method of expressing these as increments over the load of genetic disorders occurring spontaneously in man.

Chromosome Aberrations↗
PubMed1976

Evaluation and re-evaluation of genetic radiation hazards in man. II. The arm number hypothesis and the induction of reciprocal translocations in man.

The arm number hypothesis proposed by Brewen and collagues in 1973 has been examined in the light of information thus far available from mammalian studies. In experiments with peripheral blood lymphocytes (radiation in vitro), a linear relationship between dicentric yield and the effective chromosome arm number of the species was obtained in the mouse, Chinese hamster, goat, sheep, pig, wallaby and man. However, the data are not consistent with such a relationship in several primate species (marmoset, rhesus monkey, cynomolgus monkey, squirrel monkey and the slow loris), the cat and the dog. In the rabbit, the data are conflicting. In the mouse and Chinese hamster the frequencies of reciprocal translocations recorded in spermatocytes descended from irradiated spermatogonia are in line with the expectation based on the arm number hypothesis, whereas in the golden hamster, rabbit and the rhesus monkey they are not. In man and the marmoset, the limited data are not inconsistent with a 2-fold higher sensitivity of these species relative to the mouse although they do not rule out a difference as high as 4-fold. In the guinea-pig, the situation is unclear. New data on the transmission of reciprocal translocations in mice suggest that the frequency in the F1 progeny may be close to one-quarter of that recorded in the spermatocytes of the irradiated fathers (spermatogonial irradiation) at an exposure level of 150 R, whereas at higher exposures, the reduction factor is about one-eighth, the latter being in line with the earlier finding. All these results taken together suggest that inter-specific extrapolation from the radiosensitivity of somatic cells (to dicentric induction) to that of germ cells (to translocation induction) is fraught with uncertainity at present. Certain aspects that need to be studied in more detail in the context of induced chromosome aberrations are discussed.

Animals↗
PubMed1976

[The mutagenic effect of x-rays iii. radiation genetic risks].

In the estimation of radiation genetic risks, the results must be derived from animal experiments. According to recently performed investigations, humans have almost the same mutation sensibility like mice. In risk estimations, it is necessary to take into account the factors which influence the mutation rate induced per unit dose. Risk estimations are carried out by comparing the effect per unit dose with the risk of the same effect, which is caused by unknown natural influences. The reader is reffered to data derived from humans.

Animals↗
PubMed1975

Estimation of the effects of chemical mutagens: lessons from radiation genetics.

Years of work with ionizing radiations have given us a wealth of data on radiation-induced mutations. These data, which have given insights regarding the mutational processes, should form the background for all mutagenesis work. In chemical mutagenesis, as in radiation mutagenesis, it is important to know the shape of the dose-effect curve in order to make further interpretations and calculations. It is also important to be on the constant alert for new relations that can be explored.

Animals↗
PubMed1978

[Genetic radiation burden of the population in the canton Basel-City due to nuclear medicine].

The genetically significant radiation dose is defined as the gonadal dose which, if received by every member of the population, would produce the same genetic hazard to the population as do the actual doses received by the individuals. PORETTI et al. published a value of 42.9 mrad for Switzerland as the result of X-ray diagnostic examinations in 1971. The contribution from nuclear medicine was determined with reference to special circumstances in the Canton of Basle City: the annual genetically significant dose amounted to 0.5 mrad in 1976. This value represents about 0.5% of the annual annual background radiation.

Body Burden↗
PubMed1976

Evaluation and re-evaluation of genetic radiation hazards in man. I. Interspecific comparison of estimates of mutation rates.

A detailed presentation is made of the experimental data from the various systems used by Abrahamson et al. [2] to conclude that the per locus per rad (low LET) radiation-induced forward mutation rates in organisms, whose DNA content varies by a factor of about 1000, is proportional to genome size. Additional information pertinent in this context is also reviewed. It is emphasized that the mutation rates cited by Abrahamson et al. [2], although considered as pertaining to mutations at specific loci, actually derive from a broad variety of genetic end-points. It is argued that an initial (if not sufficient) condition for sound inter-specific mutation rate comparisions, covering a wide range of organisms and detecting systems of various sensitivities, requires a reasonalbly consistent biological definition of a specific locus mutation, namely, a transmissible intra-locus change. Granting the differences between systems in their resolving power to detect intragenic change, the data cited in this paper do not support the existence of a simple proportionality between radiotion-induced intra-locus mutation rate and genome size for the different species reviewed here. Furthermore, in Drosophila melanogaster, where individual salivary gland chromosome bands (that can differ greatly in DNA content) are usually associated with individual loci or at least distinct complementation groups, radiation-induced intra-locus mutation rates are not correlated with apparent differences in the DNA content of bands. This result is incompatible with the notion that most of the DNA in a band represents a radiation-mutable target capable of eliciting the kind of mutation observed in mutation rate experiments. All these considerations argue against the validity of the hypothesis of Abrahamson et al. [2] and their generalization that, for the evaluation of genetic radiation hazards in man, we can now "extrapolate from mutation rates obtained in lower organisms to man with greater confidence" on the basis of DNA content (italics are ours).

Animals↗
PubMed1978

Protection of the mouse from genetic radiation damage by an optimal-dose-ratio combination of ATP, AET, and serotonin.

The study concerned antiradiation effects in germ-cell genetic structures produced by a combination of ATP, AET, and serotonin at dose ratio optimal for lethality namely, 45:3:1, as arrived at in our previous work. Such a combination was found to reduce by a factor of 2 the translocation yields observed after 400 R X-rays to mouse spermatogonia. In terms of animal survival, ATP has been shown to contribute little to total protection achieved by the same combination; in terms of genetic damage; however, the role of ATP proved essential. Removal of ATP from the combination led to a significant reduction in protective effect.

Adenosine Triphosphate↗
PubMed1977

Mutation frequencies in female mice and the estimation of genetic hazards of radiation in women.

The female germ cell stage of primary importance in radiation genetic hazards is the immature, arrested oocyte. In the mouse, this stage has a near zero or zero sensitivity to mutation induction by radiation. However, the application of these mouse results to women has been questioned on the ground that the mouse arrested oocytes are highly sensitive to killing by radiation, while the human cells are not; and, furthermore, that the mature and maturing oocytes in the mouse, which are resistant to killing, are sensitive to mutation induction. The present results have a 2-fold bearing on this problem. First, a more detailed analysis of oocyte-stage sensitivity to killing and mutation induction shows that there is no consistent correlation, either negative or positive, between the two. This indicates that the sensitivity to cell killing of the mouse immature oocyte may not be sufficient reason to prevent its use in predicting the mutational response of the human immature oocyte. Second, if the much more cautious assumption is made that the human arrested oocyte might be as mutationally sensitive as the most sensitive of all oocyte stages in the mouse, namely the maturing and mature ones, then the present data on the duration of these stages permit more accurate estimates than were heretofore possible on the mutational response of these stages to chronic irradiation.

Animals↗
PubMed1975

Human genetic studies in areas of high natural radiation. VIII. Genetic load not related to radiation.

The genetic load disclosed by inbreeding has been analyzed in a multiple regression model for a population involving several localities in the state of Espírito Santo, Brazil. The inbreeding load has been estimated for number of pregnancies, abortions, stillbirths, children born alive, anomalies in general, sex ratio, infant mortality, post-infant mortality, and sterility and infertility of the couple. There was no evidence of either maternal or paternal inbreeding effects on the variables analyzed. The effect of inbreeding of the zygote was significant only for anomalies in general (B = 2.29 +/- 0.45) and infant mortality (B = 3.19 +/- 1.39). The latter result must be accepted with caution because of the many environmental causes affecting infant mortality. The B/A ratio suggested a predominantly mutational load for anomalies in general (B/A = 25), but with respect to infant mortality (B/A = 6), the ratio is regarded as an underestimate because of the environmental contribution to A and therefore not supportive of the segregational interpretation.

Abnormalities, Radiation-Induced↗
PubMedDate not supplied

[Human genetics studies in areas of high natural radiation. VII. Genetic load].

Two methods to estimate the inbreeding load (Morton, Crow and Muller17 1956; Freire-Maia and Freire-Maia6 1965) are reviewed. Both are employed in the analysis of our data. Besides the total population, a sample constituted of individuals with no alien ancestral is also analysed. No clean effect of natural radioactivity, as measured by genetic load models, has been found (this is especially valid for abortions, pre-natal mortality, anomalies, and abnormalities in general). The results on stillbirths and post-natal and total mortalities are discussed, and it is concluded that most probably the differences found are due to uncontrolled concomitant variables (if not to chance alone). Further analysis are under way.

Brazil↗