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PubMedDate not supplied

Chemical protection against genetic effect of radiation in male mice.

A study was made of the protective effect of some radioprotective agents against dominant lethal mutations (DLM) in postspermatogonial stages and reciprocal translocations (RT) in spermatogonia induced by gamma-radiation. Among the radioprotective agents used, cystaphos, a combination of cystamine and 5-MOT and a mixture of 6 components proved to be most effective against DLM, and cystaphos, gammaphos and cystamine combined with 5-MOT proved effective against RT. The degree of radioprotective efficacy was relatively low. The efficacy of cystamine in protecting against RT was higher with exposure of gonocytes of 18.5-day embryos than spermatogonia of pubertal animals. The degree of the radioprotective effect varied depending on the stage of spermatogenesis, and, in all cases, it was lower than that observed in studies of protection against lethal effects of ionizing radiation.

Animals↗
PubMedDate not supplied

[Genetic and somatic effects of ionizing radiation in humans and animals (comparative aspect)].

Genetic effects of ionizing radiation in the progeny of exposed parents could be conventionally subdivided on three main types. 1. Severe developmental disorders (fetus death, stillbirth, early postnatal mortality, malformation, hereditary disease, sterility). These effects are known to be caused by so called "gross" mutations (genomic, chromosomal, those of essential genes) with dominant harmful effects. Although found in rodents, insects, fishes they have not been found in humans. The proposal is made that the higher reproductive potency of a species the higher its tolerance for defective organisms. Due to strong selection against severe defects at the earliest stage of pregnancy, this genetic effect of radiation is likely to be difficult to detect in people. 2. Increased cancer risk manifested as elevated incidence of spontaneous tumors and increased sensitivity to carcinogenic agents. 3. Decreased fitness (non-carcinogenic negative health effects). These two last types of radiation genetic effects are presumably due to instability and functional inferiority of cell genome in the progeny of irradiated parents. The genetic background of these effects is suggested to be the load of induced minor mutations in regulatory genes (mini-, microsatelite loci) or/and epigenomic rearrangements of DNA in parental germ cells transmitted to progeny. These radiation genetic effects are much more obvious in animals as compared to humans. Apparently, they are difficult to find in humans because of their essential dependence on promotive (life style) factors, which are impossible to control in the offspring of irradiated people. A comparison of somatic (in irradiated organisms) and genetic (in the progeny of irradiated parents) effects of radiation provide evidence on the phenomenological as well as pathogenic similarity.

Animals↗
PubMed1999

The human vitamin D receptor gene (VDR) is localized to region 12cen-q12 by fluorescent in situ hybridization and radiation hybrid mapping: genetic and physical VDR map.

The vitamin D receptor (VDR) is a member of the steroid hormone receptor superfamily of ligand-activated transcription factors. The VDR gene was previously mapped to human chromosome 12q13-12q14, but its precise physical and genetic localization are unknown. The present study reports the mapping of the human VDR gene by radiation hybrid (RH) analysis, the isolation of a bacterial artificial chromosome (BAC) containing this gene, and physical mapping of the VDR gene by fluorescent in situ hybridization (FISH). RH analysis placed the VDR gene locus at chromosome 12cen-q12, flanked by Stanford Human Genome Center (SHGC) 30216 and SHGC 9798 (D12S1892) markers. FISH analysis of a BAC containing the VDR gene confirmed its centromeric location. Thus, we have identified a BAC and genetic markers which can be used in the genetic analysis of the VDR gene and investigation of its involvement in osteoporosis and related disorders. We conclude that the VDR gene is centromeric to its previously reported locus on chromosome 12.

Centromere↗
PubMed1996

Genetic complementation of radiation response by 3' untranslated regions (UTR) of RNA.

The molecular basis of radiosensitivity was studied using a cDNA complementation approach to correct radiosensitivity in cells. Four cDNAs of sizes 1.6, 2.0, 2.2 and 2.5 kb were isolated that corrected several aspects of the phenotype of cells from patients with the human genetic disorder ataxia-telangiectasia, characterized by hypersensitivity to ionizing radiation. The criteria used to assess correction included cell viability, induced chromosome aberrations, G2 phase delay and induction of p53 after exposure to radiation. One cDNA (2.5 kb) was identified as the complete sequence of the RNA helicase p68, which was capable of correcting radiosensitivity based on two of the above four criteria, with p53 induction post irradiation being partially corrected. The 2.2 kb cDNA was shown to correspond to the complete sequence of arginyl tRNA synthetase and the other two cDNAs were identical to the 3' untranslated regions (UTR) of the transcription factor TFIIS (1.6 kb) and phospholipase A2 (2.0 kb) respectively. Additional transfections with the 3'UTR (198 nucleotides) of p68 RNA helicase and its inverse sequence revealed that the 3'UTR had the same complementation capacity as the full-length cDNA, whereas the inverse construct failed to complement radiosensitivity. These data provide additional support for a novel role for 3'UTRs in the regulation of gene expression.

Ataxia Telangiectasia↗
PubMedDate not supplied

[Modification of the genetic effect of radiation in mice exposed in the region of the Chernobyl Atomic Electric Power Station].

A study was made of the protective effect of beta-carotine and ephasol against genetic damages in germ cells of male mice, exposed within the zone of Chernobyl NPP or ingested by 137Cs. The analysis of reproductive function, frequencies of dominant lethal mutations, abnormal sperm heads, reciprocal translocations and testis mass decrease show that both agents are more effective in protection against reproductive function damages than against genetic effects.

Animals↗
PubMed1997

[Genetic predisposition and radiation sensitivity of normal tissue].

BACKGROUND: After radiotherapy there are always some patients who develop strong acute and late reactions in normal tissues. In these patients frequently a genetic predisposition is observed. There are found DNA-repair deficiencies and changes in the regulation of the cell cycle which are responsible for the increased radiosensitivity with enhanced cell killing. METHODS: The micronucleus test and the comet assay appear to be appropriate tests in order to measure this increased radiosensitivity. Both tests are characterized by being relatively quick and simple and can be performed with small cell numbers. It is possible to study blood lymphocytes and fibroblasts with these tests. RESULTS: Both tests can predict the radiosensitivity of normal tissues especially if they are applied in combination. CONCLUSIONS: Epidemiological studies with patients after radiotherapy show evidence that the increased radiosensitivity also causes an enhanced induction of secondary tumors by ionizing radiation. This is supported by corresponding animal models.

Ataxia Telangiectasia↗
PubMed2002

Genetic regulation of ionizing radiation sensitivity and breast cancer risk.

Genetic variability in DNA repair may contribute to hypersensitivity to ionizing radiation (IR) and susceptibility to breast cancer. We used samples collected from a clinic-based breast cancer case-control study to test the working hypothesis that amino acid substitution variants of DNA repair genes may contribute to prolonged cell-cycle delay following IR and breast cancer risk. Fluorescence-activated cell sorter (FACS) analysis was used to measure cell-cycle delay. PCR-restriction fragment length polymorphism (RFLP) assays were used to determine four genotypes of three DNA repair genes: XRCC1, 194 Arg/Trp and 399 Arg/Gln; XRCC3, 241 Thr/Met; and APE1, 148 Asp/Glu. The data showed that breast cancer patients had a significantly higher delay index than that of controls (P < 0.001); the means +/- SD for cases and controls were 36.0 +/- 13.1 (n = 118) and 31.4 +/- 11.5 (n = 225), respectively. There was a significant dose-response relationship between delay index, categorized into quartiles, and an increasing risk of breast cancer (crude odds ratios: 1.00, 1.00, 1.27, and 2.46, respectively; P(trend) = 0.002). In controls, prolonged cell-cycle delay was significantly associated with the number of variant alleles in APE1 Asp148Glu and XRCC1 Arg399Gln genotypes (P(trend) = 0.001). Although larger studies are needed to validate the results, our data suggest that an inherited hypersensitivity to IR may contribute to human breast carcinogenesis.

Adolescent↗
PubMed2005

Radiation hybrid and genetic linkage mapping of two genes related to fat metabolism in cattle: fatty acid synthase (FASN) and glycerol-3-phosphate acyltransferase mitochondrial (GPAM).

Fatness traits, such as fat deposition, carcass composition, fat content, and the percentage of fat in milk, are economically relevant to cattle production. Fatty acid synthase (FASN) and glycerol-3-phosphate acyltransferase mitochondrial (GPAM) are two enzymes that play a central role in de novo lipogenesis. Both could be putative candidate genes for quantitative trait loci (QTL). Several clones containing the fatty acid synthase (FASN) and glycerol-3-phosphate acyltransferase mitochondrial (GPAM) genes were isolated after screening the INRA bovine bacterial artificial chromosome (BAC) library using PCR. Five microsatellite loci were derived from the BAC clones containing the genes of interest with heterozygosity values ranging from 27 to 78%, using DNA samples from the International Bovine Reference Panel (IBRP). The newly developed markers were genotyped on the IBRP animals and on a radiation hybrid panel to compare the obtained linkage and RH maps. Radiation hybrid maps were developed for chromosome BTA19 and BTA26 regions containing FASN and GPAM genes, respectively. The two genes and their associated microsatellite markers were located on the genetic or RH maps or on both. These microsatellite markers could be useful to study the QTL effect on fat synthesis in reference population.

Animals↗