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At least 181 records · Page 10Linked to original sources
PubMed1996

Clonal analysis of delayed karyotypic abnormalities and gene mutations in radiation-induced genetic instability.

Many tumors exhibit extensive chromosomal instability, but karyotypic alterations will be significant in carcinogenesis only by influencing specific oncogenes or tumor suppressor loci within the affected chromosomal segments. In this investigation, the specificity of chromosomal rearrangements attributable to radiation-induced genomic instability is detailed, and a qualitative and quantitative correspondence with mutagenesis is demonstrated. Chromosomal abnormalities preferentially occurred near the site of prior rearrangements, resulting in complex abnormalities, or near the centromere, resulting in deletion or translocation of the entire chromosome arm, but no case of an interstitial chromosomal deletion was observed. Evidence for chromosomal instability in the progeny of irradiated cells also included clonal karyotypic heterogeneity. The persistence of instability was demonstrated for at least 80 generations by elevated mutation rates at the heterozygous, autosomal marker locus tk. Among those TK- mutants that showed a loss of heterozygosity, a statistically significant increase in mutation rate was observed only for those in which the loss of heterozygosity encompasses the telomeric region. This mutational specificity corresponds with the prevalence of terminal deletions, additions, and translocations, and the absence of interstitial deletions, in karyotypic analysis. Surprisingly, the elevated rate of TK- mutations is also partially attributable to intragenic base substitutions and small deletions, and DNA sequence analysis of some of these mutations is presented. Complex chromosomal abnormalities appear to be the most significant indicators of a high rate of persistent genetic instability which correlates with increased rates of both intragenic and chromosomal-scale mutations at tk.

B-Lymphocytes↗
PubMed1993

A combined genetic and radiation hybrid map surrounding the Treacher Collins syndrome locus on chromosome 5q.

The distal region of chromosome 5q contains a large number of genes, including those implicated in a variety of Mendelian disorders. One of these, Treacher Collins syndrome (TCOF1), is an autosomal dominant disorder of craniofacial development the features of which include conductive hearing loss and cleft palate. Previous studies have localized the TCOF1 locus between D5S519 (proximal) and SPARC (distal). To more accurately define the genetic distance between these markers, and to extend a high resolution genetic map of 5q31-33 to include additional highly informative markers, 15 loci (including polymorphisms for 4 known genes) were mapped through the Centre d'Etude du Polymorphisme Humain reference pedigrees. The resulting genetic map encompasses 29 cM on the sex-averaged map. To help integrate this linkage map with a physical map of the region, 13 loci from 5q31--33, including 6 genes, were used to construct a radiation hybrid map. As eight of the loci are common to both maps this has allowed us to combine the maps. The most likely location for the TCOF1 locus within this marker framework is in the D5S519-SPARC interval; a region estimated to be approximately 880 kb.

Animals↗
PubMed1984

Perspective on genetic effects of radiation.

The BEIR -III estimates of genetic effects of radiation are combined with current estimates of radiation from the nuclear-energy industry to derive estimates of the genetic effects of the latter, and the results are put into perspective. All nuclear electricity would have genetic effects equivalent to those of increasing average parental age by 2.6 days (average age of parents shifted by 1.8 yr between 1940-1960), or of men spending 8 hr more per year wearing pants . If 0.5% of the taxes paid by the nuclear industry were used to combat genetic disease by currently available methods, this would avert 160 cases of genetic disease for each case caused by the nuclear industry. Using this money for genetic research would be even more profitable, by a large factor. It is pointed out that the activities of our generation have numerous impacts, both favorable and unfavorable, on future generations that are enormously more important than the genetic effects of our radiation. It is shown that the genetic effects of radiation cannot destroy the human race or create new type monsters. Genetic risks to children of radiation workers and non-radiation workers in the present generation are also treated.

Abnormalities, Radiation-Induced↗
PubMed1994

Considerations for evaluating ultraviolet radiation-induced genetic damage relative to Antarctic ozone depletion.

Springtime ozone depletion over the Antarctic results in increased UVB in local marine environments. It has been established that decreases in primary productivity occur with decreases in ozone concentrations, but the impact of increased UVB on the functioning and stability of the ecosystem has not yet been determined. Very little has been done to evaluate the potential for genetic damage caused by the increase in UVB, and this type of damage is most significant relative to the fitness and maintenance of populations. An essential problem in evaluating genotoxic effects is the lack of appropriate techniques to sample and quantify genetic damage in field populations under ambient UVB levels. In addition, it is currently not feasible to estimate exposure levels for organisms in their natural habitats.

Animals↗
PubMedDate not supplied

[Radiobiological research at the Joint Institute for Nuclear Research (JINR)].

The Joint Institute for Nuclear Research has the unique sources of ionizing radiation. The different radiobiological researches have been carried out at the JINR accelerators for more than forty years. They are connected not only to the solution of fundamental problems of radiation genetics but also with applied tasks of great social importance. These tasks are concerned with the improvement of targeted therapy methods for treatment of cancer diseases.

Academies and Institutes↗
PubMed2002

The genetics of radiation-induced osteosarcoma.

Individual genetic variation can influence susceptibility to the carcinogenic effects of many environmental carcinogens. In radiation-exposed populations those individuals with a greater genetically determined susceptibility would be at greater risk of developing cancer. To include this modification of risk into radiation protection schemes it is necessary to identify the genes responsible for determining individual sensitivity. Alpha-particle-induced osteosarcoma in the mouse has been adopted as a model of human radiation carcinogenesis, and genome-wide screens have been conducted for allelic imbalance and genetic linkage. These studies have revealed a series of genes involved in determining the sensitivity to radiogenic osteosarcoma formation.

Bone Neoplasms↗
PubMed2002

Utility of chromosomal position of heterochromatin as a biomarker of radiation-induced genetic damage: a study of Chornobyl voles (Microtus sp.).

Biomarkers that effectively document effects of chronic multi-generational exposure to contaminated environments on chromosomes would be valuable in risk assessment, remediation, and environmental decisions. Native, free-ranging populations of voles inhabiting the highly radioactive regions surrounding Reactor 4 of the Chornobyl Nuclear Power Station provide a model system to evaluate biological and chromosomal effects of chronic multi-generational exposure to radioactivity and other reactor meltdown-related pollutants. Here, we explore the utility of heterochromatic elements as potentially informative biomarkers for genetic damage in voles from the radioactive environments surrounding Chornobyl. We analyzed chromosomal positions of heterochromatin from Microtus arvalis and M. rossiaemeridionalis using fluorescent in situ hybridization. Although intrapopulational variation existed in chromosomal position and abundance of heterochromatin, none of that variation could be assigned to environmental exposure.

Animals↗
PubMed2000

Evidence that chlorophyllin (CHLN) may behave as an inhibitor or a promoter of radiation-induced genetic damage in somatic cells of drosophila.

Irradiation of 96h old Drosophila following a 24h pretreatment with 5% chlorophyllin (CHLN) was delayed 0-4 days. The antimutagenic effect of CHLN in somatic cells monitored by the wing spot test persisted for 3 days after completion of the pretreatment and appeared to terminate at a time corresponding to the cessation of mitotic divisions of wing anlagen cells. Within the same population of cells, CHLN demonstrated both an inhibitory effect as measured in mwh single spot classes, and contrarily, a promoting effect in the class of mwh/flr twin spots and to an extent in the class of large flr spots. The reason for the contrasting effects of CHLN remains to be determined.

Animals↗