MUTATION PROCESS IN CHRONICALLY IRRADIATED BANK VOLE POPULATIONS INDICATES THE TRANSGENERATIONAL GENOMIC INSTABILITY INDUCED BY CHERNOBYL FALLOUT

 

European Radiation Research 2004, August 25-28, Budapest, Hungary

http://www.osski.hu/err2004

 

R. I. Goncharova, N. I. Ryabokon : Institute of Genetics and Cytology, National Academy of Sciences of Belarus Akademichnaya st, 27. Minsk 220072, Republic of Belarus;

e-mail:  R.Goncharova@igc.bas-net.by

 


 

The objective of this investigation is analysis of mutagenesis dynamics in bank vole populations chronically exposed to low doses of ionizing radiation in connection with the absorbed dose dynamics and the number of affected generations over 19861996.

Frequencies of different end-points (chromosome aberrations in bone marrow cells and embryonic mortality) as well as the dose rate and absorbed doses of external and internal irradiation from caesium isotopes were determined for four populations inhabiting the sites with different ground deposition of 137Cs (81526 kBq/m2).

It has been first revealed that the main feature of mutagenesis dynamics in populations of mammals chronically exposed to very low doses of ionizing radiation is a gradual increase in the rate of somatic mutagenesis and embryonic lethality over 122 generations. At the same time, the dose rate and whole body absorbed dose decreased in every consecutive generation after the primary radiation insult in 1986.

The data on chromosome aberrations and embryonic lethality were fitted by the exponential and linear functions respectively. It means that genomes of animals from distant generations are more sensitive to the impact of very low radiation doses in comparison with those of animals of prior generations. The fact that dynamics of somatic mutagenesis (by the chromosome aberration frequency in bone marrow) and embryonic lethality during the period of the study closely resemble each other is an additional proof for the persistence of the delayed response.

Thus, enhanced response of distant generations of mammals to low doses of ionizing radiation is likely to be due to transgenerational genomic instability.

Abstract 66