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PubMed1991

[Genetic injuries caused by radiation and other harmful environmental pollutants].

Cancer may be induced by chemicals, ionizing radiation and certain viruses. The first causal relationships between occupation and increase in cancer have been reported two and half centuries ago. In the meantime, many other occupational toxicants have been identified as cancer inducing agents. However, quantitative risk estimates can be established in a few cases only. On the other hand, modern epidemiological investigations have brought about the main causes of cancer in highly civilized populations as certain life-styles; approximately 35% are attributed to inadequate diet and nutrition, 30% to tobacco, 7% are hormone-related in context with human reproduction, 4% due to occupational exposures, 3% may be caused by alcohol consumption, 1,5% by UV radiation and 1% by medicines (cytostatics included). Cancer risks from radiation exposure are comparatively very low. Although radiation can be measured precisely and reliably as physical units, cancers induced by nuclear weapon fallout and precipitation from the accident of Chernobyl will never be detected by epidemiological methods due to their minimal proportions. The attribution of causes obtained in this way allows for the conclusion: human cancers are mostly due to chemically definable factors, and thus are avoidable.

Carcinogens, Environmental↗
PubMed1958

Radiation dose rate and mutation frequency.

New data have clearly confirmed the earlier finding that specific locus mutation rates obtained with chronic gamma irradiation of spermatogonia are lower than those obtained with acute x-rays. Since this result is in contrast to classical findings for Drosophila spermatozoa, and apparently contradicts one of the basic tenets of radiation genetics, it was important to determine what factors were responsible for it. Experiments undertaken for this purpose reveal the following: (i) the lower mutation frequency is due mainly to difference in dose rate of radiation, rather than quality; (ii) a dose-rate effect is not obtained in experiments with mouse spermatozoa, confirming classical findings for spermatozoa, and indicating that the explanation for intensity dependence in spermatogonia resides in some characteristic of gametogenic stage; and (iii) a dose-rate effect is found not only in spermatogonia but also in oocytes, where cell selection is improbable, indicating that the radiation intensity effect is on the mutation process itself. A threshold response for all mutations in spermatogonia and oocytes is not a necessary consequence of the findings. Plausible hypotheses consistent with the present results can lead to other predictions. From a practical point of view, the results indicate that the genetic hazards, at least under some radiation conditions, may not be as great as those estimated from the mutation rates obtained with acute irradiation. However, it should not be forgotten that even the lower mutation rates obtained with the present intensity levels are still appreciable (16).

Animals↗
PubMed1998

Genetic instability in radiation-induced leukaemias: mouse models.

PURPOSE: Genetic instability plays a major role in multi-stage carcinogenesis. Ionizing radiation induces delayed genetic instability which can be transmitted to the clonal offspring of the irradiated cell, so it is of considerable importance to determine whether radiation-induced genetic instability contributes to radiation-leukaemogenesis. RESULTS: The experimental data obtained using radiation-induced leukaemias in mouse models were reviewed, and an attempt was made to distinguish between the instability detectable in de novo cancers and that which is associated with ionising radiation. Genetic lesions identified in mouse leukaemias include non-clonal chromosomal aberrations, loss of heterozygosity, and minisatellite/microsatellite mutations. CONCLUSIONS: Studies of mouse radiation-induced leukaemias have detected evidence of genetic instability. However, with few exceptions, most of this instability was also observed during de novo multi-stage carcinogenesis. This raises the possibility that radiation induces ongoing genetic instability that is functionally indistinguishable to that implicated in de novo tumour progression.

Animals↗