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At least 937 records · Page 52Linked to original sources
PubMed2004

A genome scanning approach to assess the genetic effects of radiation in mice and humans.

We used Restriction Landmark Genome Scanning (RLGS) to assess, on a genome-wide basis, the mutation induction rate in mouse germ cells after radiation exposure. Analyses of 1,115 autosomal NotI DNA fragments per mouse for reduced spot intensity, indicative of loss of one copy, in 506 progeny derived from X-irradiated spermatogonia (190, 237 and 79 mice in 0-, 3-, and 5-Gy groups, respectively), permitted us to identify 16 mutations affecting 23 fragments in 20 mice. The 16 mutations were composed of eight small changes (1-9 bp) at microsatellite sequences, five large deletions (more than 25 kb), and three insertions of SINE B2 or LINE1 transposable elements. The maximum induction rate of deletion mutations was estimated as (0.17 +/- 0.09) x 10(-5)/locus Gy(-1). The estimate is considerably lower than 1 x 10(-5)/locus Gy(-1), the mean induction rate of deletion mutations at Russell's 7 loci, which assumed that deletion mutations comprise 50% of all mutations. We interpret the results as indicating that the mean induction rate of mutations in the whole genome may be substantially lower than that at the 7 loci. We also demonstrate the applicability of RLGS for detection of human mutations, which allows direct comparisons between the two species.

Animals↗
PubMed1975

Genetic control of radiation sensitivity and DNA repair in Neurospora.

Radiation sensitivity in the fungus Neurospora crassa is under the control of at least eight distinct loci and is also affected by cytoplasmic factors. Although radiation-sensitive mutants which affect inter- or intragenic meiotic recombination have not been isolated, mutants which are defective in the repair of pyrimidine dimers have been found. Evidence from both mutational and biochemical studies shows that Neurospora has an excision-repair system for pyrimidine dimers which is very similar to the one found in Escherichia coli. Wild-type strains excise dimers, but two mutants, uvs2 and upr1, are UV sensitive and excision defective. Like the E. coli excision-defective mutants, the Neurospora mutants show a greatly increased frequency of UV-induced mutation at low UV doses, and they do not affect recombination. However, they differ from the E. coli mutants in being significantly more sensitive to ionizing radiation than wild-type strains. A third mutant, uvs6, resembles the DNA polymerase-I-negative mutants of E. coli. It is sensitive to both UV and X-irradiation, has a wild-type pattern of UV-induced mutation, and increases spontaneous deletion frequencies. Its polymerases have not been examined. The high frequency of UV-induced mutation in excision-defective strains suggests that a "mutation prone" system of DNA repair exists in Neurospora. This is supported by the ppoperties of the uvs3 strain, which shows no UV-induced mutation. Like postreplication-repair-defective E. coli mutants, it is UV and ionizing radiation sensitive and sensitive to both monofunctional and bifunctional alkylating agents. This mutant is sterile. As expected, the double mutant uvs3 upr1 strain is much more sensitive to UV than either single-mutant strain. Two other loci, muc2 and gs6, may affect DNA repair. Mutations at the five remaining loci, uvs1, uvs4, uvs5, gs3, and gs20, lead to a constellation of properties unlike those of any DNA-repair-deficient E. coli mutant. The occurrence of these mutations could mean that other DNA repair systems exist in Neurospora, or, like the lon mutants of E. coli, they might indicate that cell sensitivity to radiation damage can be increases in other ways.

DNA↗
PubMed2003

James Neel and the doubling dose concept.

The doubling dose (DD) is a very valuable concept in attempts to assess the genetic risks of radiation in man. It was long thought that the value of the doubling dose obtained from specific locus experiments in mice could be applied to man. James Neel, as a result of his studies on the offspring of atomic bomb survivors, showed that this was not so, but that different doubling doses could be inferred from different endpoints.

Animals↗
PubMedDate not supplied

[Ability of energy metabolism of cells to activate repair of its genetic material after radiation damage].

A new hypothesis on a mechanism of action of the radioprotective and medical preparations involving the activation of oxidative phosphorylation and biogenesis of mitochondria which provides the increase of dimension and rapidity of the cellular reparation has been suggested. A previously unknown property of mitochondrions to determine a cellular homeostasis has been found. An activation of oxidative phosphorylation of mitochondria is a way of cellular protection against extreme conditions (namely, against radiation exposure and tumor formation).

Adenosine Diphosphate↗