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SEL’SKOKHOZYAISTVENNAYA BIOLOGIYA
[AGRICULTURAL BIOLOGY], 2015, V. 50, № 2, pp. 225-236 issn 2313-4836 (Online)
Radiation biology, protection technologies
UDC 636.5:591.1:539.1.047 doi: 10.15389/agrobiology.2015.2.225rus
doi: 10.15389/agrobiology.2015.2.225eng
ABNORMALITIES IN THE OFFSPRING OF HENS SUBJECTED TO CHRONIC EFFECT OF 131I
V.A. BUDARKOV
All-Russian Institute of Veterinary Virology and Microbiology, Russian Academy of Agricultural Sciences, Pokrov, Petushinskii Region, Vladimir Province, 601120 Russia, e-mail budarkovva@yandex.ru Received November 17, 2014
Abstract
Modern radiobiology and medicine is faced with distant consequences of 131I chronic effects on descendants of animals and people suffered from the Chernobyl’ accident. Different disturbances in embryogenesis and congenital malformations are observed in the offspring of those whose thyroid gland was exposed to irradiation with 131I. Nevertheless, a long term prediction of 131I chronic effect in multiple generations is not still cleared up. So, we studied abnormalities of development in seven generations of offsprings which were obtained from Russian white hens subjected to chronic influence of 131I during 30 day administration of the isotope at equal daily doses of 0.11, 1.1, 2.1 and 4.6 mBq/kg. A total of 2573 offspring chickens were obtained 3, 6 and 12 month after the isotope administration has been started, and then they were surveyed for 1.5 to 2.5 years and compared to 2782 control chickens of the same age whose parents were not subjected to irradiation. The offspring of 131I radiation-exposed poultry was characterized by higher postnatal death rates, accelerated sexual maturation which was expressed in an earlier molding and 1st egg laying time, as well as with some decrease in body weight of mature birds for the majority of the generations. The offspring of the first three poultry generations from the group exposed to 131I at a dose of 1.1 mBq/kg had tumors on the jaws, neck and/or conjunctiva. Among the chicken generations 4 and 5, the degenerates appeared at a frequency of 0.75% with abnormalities mostly manifested as head defects (e.g., absence or deformation of eyes or X-shaped jaw decussations). The first four offspring generations older than 6 months being under test exhibited tumors similar to lymphoreticulosarcoma in soft tissues at a frequency from 0.8 to 4.7%. Chickens death in the experimental groups resulted mainly from disorders of gastrointestinal tract, liver, heart and kidney. An increased mortality seemed to be related with changes occurred in the course of embryogenesis leading to improper regulation and adaptation in early postnatal period.
Keywords: incorporated 131I, hens, offspring, developmental abnormalities.
Research into the remote effects of the chronic exposure of animals and people to the radiation of iodine radionuclides on the health of their offspring is one of the topical and complex problems of radiobiology and medicine [1-4]. The importance of such research is explained by the increased interest in the problem after the Chernobyl accident [5-7].
Experimental and epidemiological investigations showed that the parents’ thyroid gland exposed to radioactive iodine can cause various disorders in the process of embryogenesis and congenital malformations in the offspring (8—10). However, since data on teratogenic impact of incorporated radionuclides are incomplete, this problem should be further investigated [11-15]. For example, long term predictions of the effects of a chronic exposure to radioactive iodine isotopes on multiple generations are still not clear [16].
The purpose of this work was to investigate congenital abnormalities in the offspring of chickens after a chronic exposure to 131I.
Technique. The subjects of the research performed under vivarium conditions were Russian white chickens and seven generations of their offspring. The parent stock was split into 4 experimental (42-57 birds in each, 183 chickens in total) and 4 control (30-47 birds in each, 150 chickens in total) groups.
All hens were kept with roosters in the ratio of 1 rooster per 10 hens. For 30 days, the birds in groups I, II, III and IV (experimental) received 131I in equal portions and daily doses of 0.11, 1.1, 2.1, and 4.6 MBq/kg correspondingly. The control chickens of the same age received usual nonradioactive water in the same amounts. The birds received the isotope in February and March in the morning before feeding.
A total of 7 generations of offspring were obtained from the hens of the parent stock 3, 6, and 12 months after the beginning of isotope administration (6 generations were studied). For 1.5-2.5 years, the general condition and survival rate of each generation were monitored. The body weight was taken at the age of 1, 10, 20, 30, 40, 50, 60 days and 3, 6, 9, 12, 18, 24 months. Only 10 chickens in each group were weighed before they were 30 days old, with all the birds weighed on all the other dates.
The juvenile molt was estimated by the change of the primary feathers in 3, 4, 5-month-old chickens [17]. The intensity of the molt in all mature birds was studied during September, October and November by the change of the primary feathers.
Postmortem investigations of the internal organs were performed on the killed and died offspring [18]. In each group, 3-5 chickens were killed at the age of 1 day, 1, 3, 6 and 12 months by bleeding. After a macroscopic examination, the internal organs were weighed. The tissue samples taken from liver, spleen, kidneys, heart, thyroid gland, adrenals, and testes were fixed in 10 % solution of neutral formalin and embedded in paraffin. The histological sections were stained with hematoxylin and eosine and using Van Gieson staining protocol.
The experimental data were processed using a standard analysis of variance [19].
Results. In total, 2,573 experimental and 2,782 control offspring chickens were obtained from the hens (Fig. 1).
P *Fi(0,113)
(0,11 MBq/kg ~"-'kFi(0,ll12) —► F2—*-Бз—>-F4
P
(1,1 MBq/kg
Fi(l,l3) ■Fid.l6) ■Fid,!12)
F2—► F3—► Г4—► Fs—»F6—*- F7 F2— f3—f4— F5— F6
P -
(2,1 MBq/kg
>F1(2,13)
-Fa,!12)
F2
p -----------* Fj(4,63)
(4,6 MBq/kg
Fig. 1. Obtaining offspring from the Russian white chickens damaged by 131I: P — parents, F1-F7 — offspring of generations 1-7 (the experiment was carried out under vivarium conditions). The daily dose of 131I (MBq/kg) received by the parents is given in parentheses. The superscript indicates the number of months after the beginning of 131I administration when F1 chickens appeared
There were no differences in the appearance between 1-day-old experimental chickens in the 1st, 2nd, 3rd, 6th and 7th generations and the chickens of the same age in the corresponding control groups. Malformations, mainly in the head area, were detected in 0.75 % of 4th and 5th generations of chickens, which received 1.1 MBq/kg of 131I. An experimental chicken from the F4(1.13) group had no right eye. The jaws were deformed in an X-shape fashion (Fig. 2, А). The digits on the legs were bent, and the neck was crooked. It could hardly move
and died 2 days after hatching.
A F4(1.112) chicken had a 1.5*0.5 cm fissure on the right-hand-side of the abdominal wall covered by a transparent skin with a few feathers and light exudate under it. The abdominal organs could be clearly seen. Later on, by day 6, the fissure was replaced by a 1.5*0.5 cm cicatrix. The chicken died
7 days after hatching.
A
a
B
Fig. 2. Pathologies in the development of offspring of Russian white chickens damaged by 131I: А —
a missing eye and deformation of jaws in a F4(1.13) chicken, B — a tumor on the neck of a F2(1.112) chicken at the age of 11 months (the experiment was carried out under vivarium conditions). The daily dose of 131I (MBq/kg) received by the parents is given in parentheses. The superscript indicates the number of months after the beginning of 131I administration when F1 chickens appeared.
In the same F4(1.112) group, one chicken hatched with its eyes closed. Opened by force, the eyes could reveal a pupil through a narrow gap. The chicken died 1 day after hatching.
The left eye of a F5(1.13) chicken, which lived for 18 days, was located lower than the right one and represented a swollen round lump the size of a hazelnut with dough-like consistency. The pupil could be hardly seen through a narrow gap.
No deviations were noted in the body structure of other hatched experimental and control chickens.
The changes in the appearance of the experimental birds were observed at the age of 7-21 months. They only appeared in the first three offspring generations of chickens damaged by 131I at the dose of 1.1 MBq/kg and were represented by neoplasms on jaws, neck and conjunctiva. The neoplasms were registered in relatively young (7-12 months) F1 and F2 birds and in older (20-21 months) F3 birds (see Fig. 2, B). No similar abnormalities were noted in other experimental and control offspring groups.
The body weight of 1-day-old experimental chickens increased in Fx(0.1112), Fx(1.16), Fx(2.112), F3(0.1112), F5(1.112) groups and decreased in Fx(1.13), F2(1.13), F2(1.112), F2(2.112), F3(1.13), F4(1.13) groups compared with the control chickens. For the next 18-30 months of life, starting from puberty period, the offspring of the radiation-exposed chickens (both hens and roosters) demonstrated reliably lower weight gains than the offspring from the healthy parents.
The juvenile molt in the experimental and control chickens in all the experimental generations did not start until they were 30 days old.
The 3-month-old experimental and control F1, F2 and F3 hens from group 0.1112 did not show essential differences in the amount of replaced primary feathers. For F2 roosters from the same group the replacement of feathers was reliably more intense than in the control roosters. In group 1.13, the amount of replaced feathers increased in F5 experimental chickens compared with the control. The amount of replaced flight feathers was reliably lower in F2(1.112) experimental hens and higher in Fx(1.112) roosters. Group 2.112 was characterized by the accelerated replacement of primary feathers in both F2 hens and roosters (Р < 0.05).
According to the obtained data, the offspring of the chickens exposed to various doses of 131I molted more intensely than the control chickens. Deviations in the offspring molt depended on the time passed from the beginning of the radiation exposure of the parents: the molt was accelerated in the first generation of birds, and delayed in the subsequent generations.
The control and experimental hens started laying eggs at the age of 5.5 and 6.0 months. Three generations of experimental hens from group 0.1112 reached reproductive age at the same time as the control groups. F1(1.13) offspring reached it 14 days earlier than the control hens, and it was 3 days earlier for F2(1.112) offspring, 32 days earlier for F3(1.112), 6 days earlier for F4(1.13), and 16 days earlier for F4(1.112). F1 offspring of the chickens which received 131I at the dose of 2.1 MBq/kg started laying eggs 20 days later. The molt in Fx(1.23) chickens was more intense, and in F2(1.23) and F3(1.23) groups it was more prolonged than in the control groups. Slower molt was also noted in the experimental offspring from group 1.212.
Both experimental and control offspring showed similar dynamics of age-related changes in the internal organs. Up to the age of 6 months, no deviations in the morphology of the internal organs were noted in the killed birds. Pathological changes, which were not observed in the control groups, were found in died and killed experimental chickens of older age.
A B
Fig. 3. Heart pathology in a 7-month-old F2(2.13) rooster of the Russian white chicken damaged by 131I: А — a general view of a torose enlarged heart, B — a microphotograph of heart tissues (proliferation of lymphoid and reticular cells, atrophy of muscle fibers can be seen; the experiment was carried out under vivarium conditions). Hematoxylin and eosine stain, magnification x400. The daily dose of 131I received by the parents was 2.1 MBq/kg; F1 chickens appeared 3 months after the beginning of the exposure to 131I.
The abnormalities in the heart structure manifested themselves as a growth of a yellow-white tissue on the epicardium, endocardium and myocardium. In case of minor lesions, there were a few nodules in the heart; in case of severe lesions, the heart became torose, its weight increased and sometimes reached 26 g (Fig. 3, А).
A histologic examination revealed infiltration of lymphoid and reticular cells between the muscle fibers of the heart. In the areas of large aggregations of these cells, only a few bundles of thinned muscle fibers with poorly defined cross striations remained (see Fig. 3, B). Cardiac pathologies in the experimental birds suggestive of leukemic damage based on their macro- and microscopic structure were registered many times: one case in each of the F1(0.1112), Fx(2.112) and F2(1.112) groups and five cases in each of the F2(1.13) and F2(2.112) groups.
Similar areas of a whitish neoplasm tissue were found in the liver on the experimental chickens. The size of the nodules in the parenchyma varied
Fig. 4. A microphotograph of reticulosarcoma in the liver of a 9-month-old chicken from F2(1.13) group, one of the offspring of the Russian white chicken damaged by 131I (the experiment was carried out under vivarium conditions). Hematoxylin and eosine stain, magnification x400. The daily dose of 131I received by the parents was 1.1 MBq/kg; Fi chickens appeared 3 months after the beginning of the exposure to 131I
from a millet grain to a hazelnut, the organ was enlarged.
Depending on the degree of the damage, a microscopic examination of the liver revealed more or less pronounced proliferation of poorly differentiated reticular and lymphoid cellular elements along the blood vessels. Bigger agglomerations of these cells looked like reticulosarcoma, with the liver tissue being fragmented, its cells in the condition of fatty degeneration and necrobiosis (Fig. 4). Such changes in the liver were identified in five cases, two of them were in F1(1.13) and three were in F2(1.13).
The most frequent disorders in the offspring of the chickens damaged by 131I were kidney morphology disorders. Atrophy of the left kidney and hypertrophy of the right kidney were observed in an experimental F2(1.112) hen and an experimental F1(1.13) rooster. In 12 cases, morphological changes in the kidneys of the experimental
chickens manifested themselves as nodules of a white tissue in the parenchyma of the organ, and as light color roundish lumps emerging on the surface, with dense consistency, the size of a hazelnut or a walnut, frequently stratified if viewed in cross section (Fig. 5). The weight of the kidneys was increased and sometimes reached 25 g.
Heavy plethora, cellular dissociation and epi-thalaxia of canaliculi, clusters of young reticular cells between the canaliculi were found during a histological investigation. In case of severe kidney lesions, these cells almost completely substituted the renal parenchyma, which indicated reticulosis. Such macro- and microscopic changes in kidneys were observed once in F1(1.13), two times in F1(1.112), once in F1(2.112), two times in F2(1.112), once in F2 (1.112), three times in F3(1.13), once in F3(1.112), and once in F4(1.13).
Morphological changes in the thyroid gland were noted in two experimental chickens from F1(2.112) and F2(1.13) groups. The thyroid glands were enlarged, torose, and anisochromatic. A histological investigation revealed a reduced number of follicles and the parenchyma of the gland substituted with lymphoid and reticular cells.
The changes in the morphology of the ovaries were noted once in each of the F1(1.13), F1(2,112), and F2(1.112) groups and twice in F2(1.13) group. The
Fig. 5. A neoplasm on a kidney of a 7-month-old F4(1.13) rooster, one of the offspring of the Russian white chicken damaged by 131I (the experiment was carried out under vivarium conditions). Hematoxylin and eosine stain, magnification x400. The daily dose of 131I received by the parents was 1.1 MBq/kg; F1 chickens appeared 3 months after the beginning of the exposure to 131I.
ovaries of these chickens had the appearance of a cauliflower, with yolk spherules colored from white to black, often with hemorrhages. A histological investigation revealed a curved structure of the organ, with aggregations of lymphoid and reticular cellular elements in the parenchyma.
Numerous yellowish nodules having elastic consistency, pea- to walnut-size, were found on the mesentery and intestine of two experimental chickens in F1(1.13) and F2(1.13) groups. A microscopic examination of the tumor-like growths revealed aggregations of reticular cells.
During an autopsy, a yellowish lump having elastic consistency, lardlike if viewed in cross section, hazelnut-size, was found on a lung of a 7-month-old F2(1.13) hen. A histological investigation revealed that the cellular composition of the neoplasm was inhomogeneous. Among the lymphoid and reticular cells, the lymphoid cells prevailed, with stromal overgrowth around the organ; the cytolysis was marked. The stated features indicated that it was lympho-reticulosarcoma.
The tumors in the thoracic cavity, the cellular composition of which was suggestive of reticulosar-coma, were found in two experimental offspring chickens. A F2(1.112) hen had a tumor the size of a chicken egg, of firm consistency, stratified if viewed in cross section, which was located next to the right lung and had grown into the intercostal muscles. Most of the thoracic cavity of a F3(1.112) hen was occupied by a tumor-like growth.
In one case, a rounded tumor the size of a chicken egg having elastic consistency, lard-like if viewed in cross section, was found on the back of a 7-month-old experimental rooster from F2(1.13) group under the skin between the wings. A microscopic examination revealed that its tissue was distinctly vascularized, a marked stroma surrounded aggregations of immature reticular cells. The structure of the tumor tissue was similar to reticulosarcoma (Fig. 6).
The offspring survival rate of 131I radiation-exposed chickens was decreased (Table 1). The highest mortality rate among the experimental chickens was noted during the 1st month of their life. By the end of the 1st month, in groups 0.1112; 1.13; 1.16; 1.112; 2.112, and 4.63 of generation F1 the number of died chickens was 10.2 %, 7.0 %, 7.8 %, 7.7 %, 41.5 %, and 45.5 % higher than in the control groups.
Decreased survival trend among the experimental F1 chickens continued into the older ages; however, much fewer chickens in the groups 0.113; 1.13; 1.112; 2.12 died than in the 1st month of their life. By the age of 18 months, the differences in the survival rates among the experimental and control birds in these groups increased by < 3 % as compared with the corresponding indicators for 1-month-old chickens. In group 4.63, the mortality rate among the experimental chickens increased progressively with their age and all of them died by the end of the 2nd month of their life.
Fig. 6. A microphotograph of a tumor on the back of a 7-month-old experimental F2(1.13) rooster, a one of the offspring of the Russian white chickens damaged by 131I (proliferation of reticular cells is observed; the experiment was carried out under vivarium conditions). Hematoxylin and eosine staining, magnification x400. The daily dose of 131I received by the parents was 1.1 MBq/kg; F1 chickens appeared 3 months after the beginning of the exposure to 131I
1. Age-related dynamics of the survival rate (%) in the offspring generations of the Russian white chickens subjected to experimental exposure to 131I in different doses (experiment under vivarium conditions)
Age 1 Group 1 F, F2 F3 1 F4 1 F5 1 F6
1 month 0.1112 69.8 78.0 76.5 - - -
Control 78.0 81.1 78.0 - - -
1.13 79.0 78.8 76.8 52.3 71.4 72.3
Control 86.0 84.7 87.2 71.2 81.7 80.3
1.16 72.2 - - - - -
Control 80.0 - - - - -
1.112 83.4 76.9 57.7 81.7 69.8 -
Control 91.1 93.7 74.3 85.3 78.0 -
2.112 36.5 59.6 - - - -
Control 78.0 81.1 - - - -
4.63 32.5 - - - - -
Control 78.0 - - - - -
2 months 0.1112 65.6 69.2 74.3 - - -
Control 75.0 79.2 73.8 - - -
1.13 77.2 75.9 71.6 51.2 66.9 47.9
Control 82.0 83.6 83.9 69.4 81.2 67.9
1.112 81.4 73.5 50.8 75.5 60.3 -
Control 90.0 90.6 67.3 83.2 73.8 -
2.112 32.4 59.6 - - - -
Control 75.0 79.2 - - - -
3 months 0.1112 65.6 69.2 72.0 - - -
Control 75.0 79.2 67.7 - - -
1.13 77.2 74.6 70.5 50.0 66.9 47.9
Control 81.3 82.6 82.6 69.4 80.3 67.9
1.1i2 80.7 73.5 49.2 75.5 60.3 -
Control 90.0 89.1 65.3 82.7 67.7 -
2.112 32.4 59.6 - - - -
Control 75.0 79.2 - - - -
6 months 0.1112 63.4 69.2 68.2 - - -
Control 73.5 78.3 67.1 - - -
1.13 74.6 67.0 69.5 46.5 66.9 46.9
Control 81.3 80.5 81.7 67.6 79.8 67.4
1.1i2 75.8 72.7 48.5 74.7 60.7 -
Control 88.9 87.5 65.3 82.3 67.1 -
2.112 32.4 59.6 - - - -
Control 73.5 78.3 - - - -
12 months 0.1112 63.4 68.9 68.2 - - -
Control 72.0 78.3 67.1 - - -
1.13 71.9 60.3 64.2 42.0 66.9 46.9
Control 78.6 77.8 79.0 64.7 79.4 65.8
1.112 71.8 64.9 43.8 72.2 60.3 -
Control 84.4 86.7 65.3 81.2 67.1 -
2.112 29.6 - - - - -
Control 72.0 - - - - -
18 months 0.1112 61.2 68.9 68.2 - - -
Control 70.5 78.3 67.1 - - -
1.13 67.6 55.5 59.9 33.6 65.7 46.9
Control 77.3 76.7 78.5 62.2 78.9 46.8
1.112 68.9 57.3 41.5 72.2 60.3 -
Control 84.4 83.6 63.4 80.7 67.1 -
2.112 28.2 - - - - -
Control 70.5 - - - - -
24 months 1.13 66.7 51.7 57.4 - - -
Control 75.9 75.1 78.5 - - -
1.112 64.0 52.3 - - - -
Control 84.4 82.3 - - - -
30 months 1.13 66.7 50.0 - - - -
Control 75.9 75.1 - - - -
1.112 62.6 - - - - -
Control 82.2 - - - - -
Note: Column «Group» shows a daily dose of 131I (MBq/kg), received by the parents. The superscript indicates the number of months after the beginning of 131I administration when F1 chickens appeared. The dashes mean that the investigation was not performed.
The next generations of the experimental birds demonstrated decreased survival rates too. By the age of 6 months, the survival rate of F2 chickens in groups 0.1112; 1.13; 1.112 and 2.112 was lower than in the control groups by 9.1 %, 13.5 %, 14.8 %, and 17.7 % correspondingly. A similar survival dynamics in the experi-
mental groups was observed in generations 3-6 too.
Weak newborn chickens, which mainly died in the 1st month of their life, represented the largest share in the total number of deaths among the control and experimental offspring.
2. Frequency of lethal outcomes depending on their causes in the generations of the Russian white chicken offspring subjected to experimental exposure to 131I in different doses (experiment under vivarium conditions)
With disorders
Generation Group Total died Born weak of gastrointestinal tract, liver heart kidneys
F1 0.1112 36 29/80.6 5/13.9 2/5.5 -
Control 20 17/85.0 3/15.0 - -
1.13 39 24/61.5 14/36.0 1/2.5 -
Control 36 21/58.3 14/39.0 1/2.7 -
1.112 54 24/44.5 25/46.3 3/5.5 2/3.7
Control 16 8/50.0 7/43.7 1/6.6 -
2.112 51 45/88.4 4/7.8 2/3.8 -
Control 20 17/85.0 3/15.0 - -
4.63 28 28/100 - - -
Control 20 17/85.0 3/15.0 - -
F2 0.1112 23 17/74.0 6/26.0 - -
Control 23 20/87.0 3/13.0 - -
1.13 118 50/42.3 58/49.0 2/1.8 -
Control 47 29/62.0 16/34.0 - -
1.112 50 27/54.0 20/40.0 2/4.0 -
Control 23 8/34.8 15/65.2 - -
2.112 23 22/95.5 - 1/4.5 -
Control 23 20/87.0 3/13.0 - -
F3 0.1112 42 31/74.0 10/23.7 1/2.3 -
Control 66 38/57.5 27/41.0 1/1.5 -
1.13 81 44/54.5 33/40.7 2/2.4 2/2.4
Control 40 24/60.0 15/37.5 1/2.5 -
1.112 76 55/72.4 20/26.3 1/1.3 -
Control 37 26/70.2 11/29.8 - -
F4 1.13 57 41/72.0 15/26.3 1/1.7 -
Control 42 32/76.2 10/23.8 - -
1.112 76 50/65.8 24/31.6 2/2.6 -
Control 38 29/76.4 8/21.0 1/2.6 -
F5 1.13 46 39/84.8 6/13.0 1/2.2 -
Control 46 40/87.0 6/13.0 - -
1.112 25 16/64.0 8/32.0 1/4.0 -
Control 54 37/68.6 15/27.8 2/3.6 -
F6 1.13 50 26/52.0 22/44.0 1/2.0 1/2.0
Control 66 38/57.5 27/41.0 1/1.5 -
Note: Column «Group» shows a daily dose of 131I (MBq/kg), received by the parents. The superscript indicates
the number of months after the beginning of 131I administration when F1 chickens appeared. Before the slash—an absolute value, after the slash a percentage of the total number of died birds is indicated. The dashes mean no registered cases of bird death.
The percentage of died young chicken in F4 and F5 in relation to F1 increased both in the experimental and control groups.
The main reason of the lethal outcomes in the offspring of 131I radiation-exposed chickens was the fact that they were born weak; the next one was disorders of gastrointestinal tract, liver, heart and kidneys. After the 6 th month, tumor-like damages developed in the soft tissues of the bodies of the experimental offspring. With respect to the total number of chickens, the frequency of such tumors was 1.1 % in F1(0.1112), 3.5 % in F1(1.13), 3.4 % in F1(1.112), 3.8 % in Fi(2.112), 4.7 % in F2(1.13), 3.4 % in F2(1.112), 1.4 % in F2(2.112), 1.0 % in F3(1.13), 0.7 % in F3(1.112), and 0.8 % in F4(1.112). On average, the percentage of neoplasms of internal organs in the 1st generation offspring, which hatched 3 months after the beginning of the parents’ exposure to 1311 in the dose of 1.1 MBq/kg, was 3.3 %, for the 2nd generation, which hatched 12 months after the exposure, it was 2.9 %. The tumors were located in skeletal muscles, thoracic and abdominal cavity organs. In their structure, the tumors were similar to lymphoreticulosarcoma or reticulosarcoma. Carcinogenic processes seemed to
become one of the factors reducing survival rates of the experimental birds.
The mortality rate among the young birds depended on the dose of 131I received by the parents, i.e. higher doses led to more deaths among the chickens than the lower ones. No dose-related distribution of frequency of gastrointestinal tract, liver, heart and kidney disorders was noted. No renal lesions or neoplasms were encountered in the control groups.
Our results correlate with experimental data obtained on rats exposed to 131I during pregnancy [20]. Physical growth and development disorders, increase in the frequency of tumors in various locations, damage to the genetic material in the germ cells were found to be possible in the offspring born from the carriers of 131I. The scientists accept that the main cause of these phenomena is ovocyte, embryo and fetus damage induced by the direct effect of radiation. The obtained data also correlate with the results of the investigation involving the offspring of people who were exposed in the Eastern-Ural and Chernobyl traces [21-26]. The analysis of the consequences of accidental and professional exposure shows that prolonged radiation exposure may result in reproductive dysfunctions, i.e. increase in the frequency of adverse pregnancy outcomes, delays in and disorders of physical development of born offspring, high mortality rate and cancer morbidity [27-33].
In the XXI century, there are much more adverse effects of a range of human activities, including ionizing radiation, on the human body and reproductive health [34, 35]. One of the challenges the scientific community is facing is a comprehensive unbiased assessment of this serious threat, scientific justification and implementation of the most efficient measures aimed at prevention and maximum mitigation of the adverse effects of radiation, which could be passed down to the next generations [36, 37].
Thus, a number of development abnormalities was found in the offspring of the chickens subjected to a chronic exposure to 131I in the doses from 0.11 to 4.6 MBq/kg. These disorders manifested themselves as decreased postnatal survival rates, reduction of body weight, congenital abnormalities, and more frequent neoplasms. An increased mortality among the offspring of 131I radiation-exposed chickens seems to be connected with the changes taking place during embryogenesis and resulting in improper regulation and adaptation in the early postnatal period. The main causes of death among the offspring of the 131I radiation-exposed chickens were disorders of gastrointestinal tract, liver, heart and kidneys. Tumors in the soft parts of the body were found in F1-F4 offspring aged 6 months or older. In their structure, the tumors were similar to lymphoreticu-losarcoma or reticulosarcoma.
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