1022-7954/05/4101- © 2005 Pleiades Publishing, Inc.
Russian Journal of Genetics, Vol. 41, No. 1, 2005, pp. 72–78. Translated from Genetika, Vol. 41, No. 1, 2005, pp. 85–92.
Original Russian Text Copyright © 2005 by Telnov.
Ecological genetic analysis of the consequences of
ionizing radiation in humans includes two major lines
of investigations. The ﬁrst, radiation genetics, analyzes
the effects of radiation on the genetic structures and
processes. The second, genetics of radioresistance,
deals with the response of the genotypes to the radia-
tion, i.e., investigates genetic differences in the reac-
tions of an organism to the effects of the ionizing radi-
ation . In recent years, a tendency towards the expan-
sion of investigations aimed at the analysis of the role
of genetic factors in the unequal radioresistance of the
biological objects has been observed [2–4].
Genetic factors with stable characteristics seem
most promising in this respect. These factors primarily
include polymorphic genetic systems that remain
unchanged during the lifetime. It has been established
that about 30% of human genome genes are polymor-
phic, i.e., are represented by two or more alleles . It
is well known that genetic polymorphism plays an
important role in different adaptive abilities and differ-
ent morbidity of the human [6–8]. This important prob-
lem, however, remains poorly investigated in relation to
human radioresistance. It should be noted that the anal-
ysis of literature data on the issue testiﬁes to the
absence of distinct methodological approaches to eval-
uation of the role of genetic factors in radiation effects
in the human. As a rule, these surveys are carried out
using individual indices, thereby excluding the possi-
bility of systematic analysis [9–11]. Apparently, receiv-
ing more objective evaluation of the role of genetic fac-
tors in the response the organism to radiation requires
investigations on different biological organization lev-
els, from molecular to population ones.
Earlier, we have shown the important role of the
genetic markers in biochemical and age changes in the
irradiated individuals [12–15]. The present study was
focused on the evaluation of the role of a number of
polymorphic genetic systems in the onset of chronic
radiation disease, predominantly caused by chronic
-radiation, in the nuclear industry workers.
MATERIALS AND METHODS
The data on the population genetic survey of
985 workers (the main group) aged 35 to 79 years, who
were occupationally exposed to external and internal
radiation while being employed at the ﬁrst Russian
nuclear plant (Mayak PA). The major occupational haz-
ard sources in the conditions of radiochemical facility
were chronic external
-irradiation and incorporation of
plutonium-239 (Pu-239) aerosols into the organism.
-exposure doses ranged from 0.1 to
0.760 cGy. In 33.1% of the individuals examined,
incorporated Pu-239 was not detected, while in the oth-
ers at the time of the latest examination, its content var-
ied in a wide range, from 0.148 to 25.27 kBq. Among
the individuals examined, 90% were Russians. A total
of 374 subjects out of the number tested were diag-
nosed with chronic radiation disease (CRD) according
to the criteria described in .
Haptoglobin (Hp) and group-speciﬁc component
(Gc-component) phenotypes were determined using
vertical electrophoresis in 5% polyacrylamide gel .
The Role of Genetic Factors in Human Radioresistance
V. I. Telnov
Southern Ural Biophysics Institute, Ozersk, Chelyabinsk oblast, 456780 Russia;
fax: (35171)7-25-50; e-mail: nelly@ﬁb.ozersk.ru
Received November 26, 2003
—The role of genetic factors in the development of chronic radiation disease (CRD), mostly caused
by occupational external
-exposure, was evaluated. The data of molecular genetic survey of a cohort of
985 workers at the nuclear power plant, the Mayak PA, were analyzed. Among the genetic markers tested, an
association between the haptoglobin (Hp) genetic system and the development of CRD was established. It was
demonstrated that the contribution of genetic factors to the CRD onset was realized not within the whole, but
in a relatively narrow dose interval (70 to 400 cGy), i.e., was relative. Furthermore, at equal irradiation doses,
relatively higher risk of CRD was observed among the Hp 2-2 phenotype carriers (1.96) compared to lower risk
among the Hp 1-1 and Hp 2-1 phenotype carriers (0.64). It was shown that with the increase of the irradiation
dose, genotypic differences in the CRD frequency decreased to the point of their complete disappearance. Com-
parison of the roles of the genetic factors in the onset of such deterministic irradiation effect as CRD, with their
roles in the onset of lung cancer in tobacco smokers revealed similar patterns. A scheme of the relationships
between the effector intensity and the differences in the genetically determined radioresistance is presented.
The data obtained do not support the idea that the survivals of the atomic bombing of Hiroshima and Nagasaki
were the most radioresistant individuals, who are not representative for evaluating the radiation risk.