Very high mutation rate in offspring of Chernobyl accident liquidators

Weinberg, Hava-Shifra; Korol, Abraham B.; Kirzhner, Valery; Avivi, Aaron; Fahima, Tzion; Nevo, Eviatar; Shapiro, Shelby; Rennert, Gad; Piatak, O.; Stepanova, Ye.; Skvarskaja, E.

doi:10.1098/rspb.2001.1650

Cited by 67 publications

(27 citation statements)

References 31 publications

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“…A so-called lowmicrosatellite-instability phenotype has been reported in cells from tissues that are either inflamed or hyperplastic and in carcinogen-induced rat mammary tumors (10,14,25,26). In addition, changes were seen in somatic cell microsatellites of offspring of individuals exposed to radiation from the Chernobyl disaster (27). The PLAP ϩ cells present in mismatch repairproficient mice may be formed by the same process that causes low microsatellite instability, and the G11 allele may respond to the same kinds of environmental insults.…”

mentioning

confidence: 89%

Modeling variation in tumors in vivo

Stringer

Larson

Fischer

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

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Transgenic mice that allow mutant cells to be visualized in situ were used to study variation in tumors. These mice carry the G11 placental alkaline phosphatase (PLAP) transgene, a mutant allele rendered incapable of producing its enzyme product by a frameshift caused by insertion of a tract of G:C base pairs in a coding region. Spontaneous deletion of one G:C base pair from this tract restores gene function, and cells with PLAP activity can be detected histochemically. To study tumors, the G11 PLAP transgene was introduced into the polyoma virus middle T antigen mammary tumor model. Tumors in these mice exhibited up to 300 times more PLAP ؉ cells than normal tissues. PLAP ؉ cells were located throughout each tumor. Many of the PLAP ؉ cells were singlets, but clusters also were common, with one cluster containing >30,000 cells. Comparison of these data to simulations produced by computer models suggested that multiple factors were involved in generating mutant cells in tumors. Although genetic instability appeared to have occurred in most tumors, large clusters were much more common than expected based on instability alone.microsatellites ͉ mutation ͉ instability ͉ mouse

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mentioning

confidence: 89%

Modeling variation in tumors in vivo

Stringer

Larson

Fischer

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

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“…In human and wild animals, several studies of the functional changes in the reproductive tract have been made as a result of Chernobyl accident, abnormalities in spermatozoa and reproductive failures have been described [7]. Additionally, Weinberg et al reported some genetic changes of unclear importance in offspring of Chernobyl accident liquidators [14,15]. Although there are some claim that its changes is caused by the psychological factors (stressful conditions), it does not yet have enough information to explain all of the serious changes.…”

Section: Reporting Studies Of Chernobyl For Domestic Animals and Humanmentioning

confidence: 99%

Cryopreservation of Cattle, Pig, Inobuta Sperm and Oocyte after the Fukushima Nuclear Plant Accident

Yamashiro¹,

Abe²,

Kuwahara³

et al. 2014

Recent Advances in Cryopreservation

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“…Epidemiological studies of parental exposure to ionising radiation and cancer risk in children have been limited to post-Chernobyl accident biomonitoring of the so called liquidators, who were removing radioactive material and of the Chernobyl plant workers (84,85). The health effects of nuclear power plants on nearby residents have not duly been investigated; this is particularly true for genome damage in children.…”

Section: Ionising Radiationmentioning

confidence: 99%

Prenatal, Early Life, and Childhood Exposure to Genotoxicants in the Living Environment

Katic

Fučić

Gamulin

2010

Archives of Industrial Hygiene and Toxicology

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Health disorders and diseases related to environmental exposure in children such as cancer and immunologic disturbances (asthma, allergies) are on the rise. However, complex transplacental and prepubertal genotoxicology is given very limited consideration, even though intrauterine development and early childhood may be critical for elucidating the cancer aetiology. The foetus is transplacentally exposed to contaminants in food and environment such as various chemicals, drugs, radiochemically contaminated water and air. Target organs of xenobiotic action may differ between the mother and the foetus due to specifi c stage of developmental physiology and enzyme distribution. This in turn may lead to different levels of clastogenic and aneugenic metabolites of the same xenobiotic in the mother and the foetus. Adult's protective behaviour is not suffi cient to isolate children from radioisotopes, pesticides, toxic metals and metalloids, environmental tobacco smoke, endocrine disrupting chemicals, and various food contaminants, which are just a part of the stressors present in a polluted environment. In order to improve legislation related to foetus and child exposure to genotoxic and possibly carcinogenic agents, oncologists, paediatricians, environmental health specialists, and genotoxicologists should work together much more closely to make a more effective use of accumulated scientifi c data, with the fi nal aim to lower cancer incidence and mortality.

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Very high mutation rate in offspring of Chernobyl accident liquidators

Cited by 67 publications

References 31 publications

Modeling variation in tumors in vivo

Modeling variation in tumors in vivo

Cryopreservation of Cattle, Pig, Inobuta Sperm and Oocyte after the Fukushima Nuclear Plant Accident

Prenatal, Early Life, and Childhood Exposure to Genotoxicants in the Living Environment

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