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At least 1,243 records · Page 69Linked to original sources
PubMed1988

Mutation induction and relative biological effectiveness of neutrons in mammalian cells. Experimental observations.

The induction of mutation by graded doses of monoenergetic neutrons was examined using the human-hamster hybrid cell system. The AL cells, formed by fusion of human fibroblasts with the gly- A mutant of the Chinese hamster ovary cells, contain the standard set of hamster chromosomes plus a single human chromosome, number 11. These cells contain specific human cell surface antigens that render them sensitive to killing by specific antisera in the presence of complement. Mutant AL cells that have lost the surface markers, however, would survive and give rise to scorable colonies. The cells were irradiated with neutrons produced at the Radiological Research Accelerator Facility of Columbia University. Doses corresponding to low, moderate, and high cytotoxicities and in energies ranging from 0.33 to 14 MeV were used. Neutrons induced a dose-dependent cytotoxicity and mutation frequency in the AL cells. Over the range of doses examined, it was found that the mutagenesis induced by neutrons was energy-dependent and the frequencies were a curvilinear function of dose for both the a1 and a2 antigenic loci examined. In comparison to gamma rays, the relative biological effectiveness (RBE) for cell lethality at the 10% survival level ranged from 5.2 for 0.33 MeV to 1.8 for 14 MeV neutrons. The RBE for mutation induction at the a1 locus, however, ranged from 30 for 0.33 MeV to 4.2 for 14 MeV neutrons at or around the lowest levels of effect examined. Results of the present study demonstrated that neutrons, when measured under conditions which permit detection of a spectrum of gene and chromosomal mutations, in fact, are more efficient mutagens than previously thought.

Animals↗
PubMed1992

Radiation-induced mitotic delay: a genetic characterization in the fission yeast.

Radiation-induced mitotic delay is under investigation in the fission yeast, Schizosaccharomyces pombe. A large range of cell cycle- and radiation-sensitive mutants of this yeast is available to facilitate this effort. Through an examination of such mutants it has been shown that the X-ray transition point and the p34cdc2 execution point are coincident; wee1- strains are not delayed by irradiation; and the radiation-sensitive mutants rad1-1, rad3-136, rad9-192, and rad17-W are not delayed by radiation or by inhibitors of DNA synthesis, including hydroxyurea. A model is proposed: Damaged DNA generates a signal to delay mitosis which is carried by the products of the rad genes to activate the tyrosine kinase p110wee1. This in turn inactivates the serine/threonine kinase p34cdc2, thereby blocking entry to mitosis. Unreplicated DNA also initiates a signal to delay mitosis which is carried by these same rad genes but, as indicated in the literature, transmission to p34cdc2 does not require p110wee1. The delay-deficient rad mutants may possess some properties of tumor suppressor genes, with implications for mutagenesis and oncogenesis.

Animals↗
PubMed2004

Thiamine prevents X-ray induction of genetic changes in human lymphocytes in vitro.

The effects of thiamine (vitamin B1) on the level of spontaneous or radiation-induced genetic changes in human lymphocytes in vitro were studied. Cultured lymphocytes were exposed to increasing concentrations of thiamine (0-500 microg/ml) and irradiated with X-rays. The DNA damage was estimated as the frequency of micronuclei and apoptotic or necrotic morphological changes in fixed cells. The results show that thiamine alone did not induce genetic changes. A significant decrease in the fraction of apoptotic and necrotic cells was observed in lymphocytes irradiated in the presence of vitamin B1 at concentrations between 1-100 microg/ml compared to those irradiated in the absence of thiamine. Vitamin B1 at 1 and 10 microg/ml decreased also the extent of radiation-induced formation of micronuclei. Vitamin B1 had no effect on radiation-induced cytotoxicity as measured by nuclear division index. The results indicate that vitamin B1 protects human cells from radiation-induced genetic changes.

Apoptosis↗
PubMed1975

[Radio-iodine treatment of hyperthyroidism. Experience in more than 2000 patients (author's transl)].

Results of radioiodine therapy (131/125) of hyperthyroidism are reported. The individually calculated doses of 131-iodine were: 6000 rad in cases of small (not more than 60 g) diffuse goiters, 8000-10000 rad in large diffuse goiters, 10000-12000 rad in nodular goiter and 30000-40000 rad in autonomous adenoma. In about 75% of the patients a single application of 131-iodine was sufficient to control the hyperfunction. The cumulative risk of myxedema ten years after therapy was: 31% in small diffe goiters, 12% in large diffuse goiters and 6% in nodular goiter. All cases considered together, the cumulative myxedema risk was about 12%. This figure compares favourably with the results of surgical treatment and they document the necessity of individual calculation of the dose in order to get optimal results. 125-iodine was applied since October 1972 in cases of small diffuse goiters. The dose was standardized according to the gland weight, uptake and effective half value time (dose at the colloid-cell interface 12000-15000 rad). 5-12 months thereafter, there were about 60% of the patients euthyroid. The genetic and somatic risk of radiation is considered quantitatively and we conclude that there is no real argument aginst radioiodine therapy of hyperthyroidism except in children and in youth. Risks and efficiency of other treatments (surgical, antithyroid drugs) are compared with the radioiodine treatment and it is concluded that radioiodine is to be preferred in the major part of the hyperthyroid patients.

Humans↗
PubMed2005

Genetic and epigenetic features in radiation sensitivity Part I: cell signalling in radiation response.

Recent progress especially in the field of gene identification and expression has attracted greater attention to genetic and epigenetic susceptibility to cancer, possibly enhanced by ionising radiation. It has been proposed that the occurrence and severity of the adverse reactions to radiation therapy are also influenced by such genetic susceptibility. This issue is especially important for radiation therapists since hypersensitive patients may suffer from adverse effects in normal tissues following standard radiation therapy, while normally sensitive patients could receive higher doses of radiation offering a better likelihood of cure for malignant tumours. This paper, the first of two parts, reviews the main mechanisms involved in cell response to ionising radiation. DNA repair machinery and cell signalling pathways are considered and their role in radiosensitivity is analysed. The implication of non-targeted and delayed effects in radiosensitivity is also discussed.

Animals↗