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At least 613 records · Page 34Linked to original sources
PubMed1994

Induction of nuclear factor kappa B after low-dose ionizing radiation involves a reactive oxygen intermediate signaling pathway.

Reactive oxygen intermediates (ROIs) have been found to be the messengers in the activation of the kappa B transcription regulator in mitogen- or cytokine-stimulated cells, operating in conjunction with or independently of various other mechanisms; these include Ca(++)-dependent and PKC-dependent cytoplasmic signaling pathways. We have recently reported that low-dose ionizing radiation induces NF-kappa B in human lymphoblastoid 244B cells. Since ionizing radiation generates free radicals in cells, we have investigated whether the ROIs generated by ionizing radiation induce NF-kappa B activity, and also whether they do so by a similar mechanism as in cells treated with PMA or H2O2. The results not only confirm a previous observation from our laboratory that low-dose ionizing radiation (0.1-2.0 Gy) activates kappa B transcription factor transiently with a maximal induction at 0.5 Gy exposure, but also demonstrate mechanistically that the activation of NF-kappa B by low-dose ionizing radiation can be inhibited considerably by the antioxidant N-acetyl-L-cysteine, indicating that at least the major part of the activation process is mediated by ROIs. These findings support the idea that ROIs can regulate the kappa B elements which in turn can serve as response elements for oxidant stress.

Acetylcysteine↗
PubMed1997

Synergistic cytotoxic effects of ether phospholipid analogues and ionizing radiation in human carcinoma cells.

BACKGROUND AND PURPOSE: There is growing evidence in recent years that the antiproliferative effects of ionizing radiation may not be exclusively mediated via DNA damage but also by interactions and alterations of cell membrane associated processes. Here, we tested the hypothesis that membrane active cytotoxic ether lipids and analogues may interact with ionizing radiation, enhancing its antiproliferative effects. MATERIALS AND METHODS: The two epithelial tumor cell lines HTB 43 and KB, and the ether lipid resistant subline KBr were treated by a combination of radiation and ether lipids. Cytotoxic effects were measured by colony forming assays and the effects on membrane phospholipids were determined by quantitative thin-layer chromatography of cell lipid extracts. RESULTS: We present evidence that some ether lipids show supra-additive cytotoxic effects with ionizing radiation. These effects seem to depend on the same structural properties of ether lipids that determine their intrinsic cytostatic and cytotoxic activity. Identical growth inhibitory results were achieved when cells were treated before, or 30 min after irradiation. Analysis of major membrane phospholipids revealed no statistically significant differences of phospholipid distribution pattern in cells exposed to both treatment modalities. CONCLUSION: Our data indicate that changes of overall membrane phospholipid composition do not seem to be the mechanism of synergistic antiproliferative activity of ether lipids and ionizing radiation.

Antineoplastic Agents↗
PubMedDate not supplied

1alpha,25-Dihydroxyvitamin D3 modulates the response of human keratinocytes to ionizing radiation exposure.

BACKGROUND: Exposure of human skin to ionizing radiation may result in various effects such as inflammation, keratosis, fibrosis and cancer. 1alpha,25-Dihydroxyvitamin D3 (1alpha,25(OH)2D3), the biologically active metabolite of vitamin D, has been shown to exert pleiotropic effects on the skin. The aim of the study was to evaluate the effect of 1alpha,25(OH)2D3 on the radiation response of human keratinocytes. MATERIALS AND METHODS: Keratinocytes (HaCaT), either untreated or pretreated with 1alpha,25(OH)2D3, were irradiated with 0-7.5 Gy. Growth curves were generated to determine cell proliferation. Cell survival was examined using a clonogenic assay. The cell surface expression of adhesion molecules was investigated by flow cytometry. RESULTS: The cell growth and clonogenic survival of irradiated keratinocytes were both significantly increased by 1alpha,25(OH)2D3. Ionizing radiation caused an up-regulation of the cell surface expression of intercellular adhesion molecule-1 (ICAM-1) and integrins beta1 (CD29), alpha2 (CD49b), alpha5 (CD49e) and alpha6 (CD49f) in keratinocytes, which was inhibited by 1alpha,25(OH)2D3. CONCLUSION: The data suggest that 1alpha,25(OH)2D3 may be a promising agent to modify the radiation reaction, thus offering new options in radiotherapy and oncology.

Calcitriol↗
PubMed2001

Tetracycline derivatives and ceftriaxone, a cephalosporin antibiotic, protect neurons against apoptosis induced by ionizing radiation.

DNA damage induced by low doses of ionizing radiation causes apoptosis, which is partially mediated via the generation of free radicals. Both free radicals and apoptosis are involved in the majority of brain diseases, including stroke, Alzheimer's disease and amyotrophic lateral sclerosis. Because previous studies have shown that tetracycline derivatives doxycycline and minocycline have anti-inflammatory effects and are protective against brain ischemia, we studied whether minocycline and doxycycline or ceftriaxone, a cephalosporin antibiotic with the potential to inhibit excitotoxicity, protect neurons against ionizing radiation in primary cortical cultures. A single dose of 1 Gy significantly increased lactate dehydrogenase release, induced DNA fragmentation in neurons and triggered microglial proliferation. Treatment with minocycline (20 nM), doxycycline (20 nM) and ceftriaxone (1 microM) significantly reduced irradiation-induced lactate dehydrogenase release and DNA fragmentation. The most efficient protection was achieved by minocycline treatment, which also inhibited the irradiation-induced increase in microglial cell number. Our results suggest that some tetracycline derivatives, such as doxycycline and minocycline, and ceftriaxone, a cephalosporin derivative, protect neurons against apoptotic death.

Animals↗
PubMedDate not supplied

Counseling patients exposed to ionizing radiation during pregnancy.

Health physicists and knowledgeable clinicians have the responsibility to counsel women of reproductive age about the reproductive risks of ionizing radiation exposure before conception or during pregnancy. It is important to realize that lay individuals have many misconceptions about the reproductive risks of ionizing radiation. Many patients who have already had or will undergo some type of radiological test are apprehensive about the reproductive and developmental risks of diagnostic radiological procedures. Epidemiological studies and animal studies indicate that high exposures of ionizing radiation can cause miscarriage, congenital malformations, growth retardation, stillbirth, and cancer. With the exception of cancer, there are threshold exposures for those outcomes, with exposures below certain radiation doses not increasing the reproductive or developmental risks. The threshold exposure for birth defects at the most sensitive stage of development is 0.2 Gy, and the threshold for growth retardation and miscarriage is even higher. However, embryonic loss can occur from low exposures during the preimplantation and presomite stages of development ("the all or none period"). This is a stage when the embryo is more likely to die than survive malformed. The most sensitive period for the induction of mental retardation is from the 8th week to the 15th week of gestation. The threshold for deterministic effects increases after early organogenesis and also as the exposure is protracted, e.g., with radionuclides or multiple radiological procedures. Awareness that the threshold dose for developmental effects increases as the fetus develops complicates counseling because we do not have definitive data on threshold exposures at all stages of gestation. Ionizing radiation exposures prior to pregnancy represent a very low risk for the increased incidence of genetic disease in the offspring of the parents who have had radiation exposures to the ovary or testes. Counseling patients requires knowledge of embryology, genetics, radiation teratology, and the principles of teratology in order for the counselor to provide sympathetic, accurate, scholarly advice.

Abnormalities, Radiation-Induced↗
PubMed2005

"Modeled microgravity" affects cell response to ionizing radiation and increases genomic damage.

The aim of this work was to assess whether "modeled microgravity" affects cell response to ionizing radiation, increasing the risk associated with radiation exposure. Lymphoblastoid TK6 cells were irradiated with various doses of gamma rays and incubated for 24 h in a modeled microgravity environment obtained by the Rotating Wall Vessel bioreactor. Cell survival, induction of apoptosis and cell cycle alteration were compared in cells irradiated and then incubated in 1g or modeled microgravity conditions. Modulation of genomic damage induced by ionizing radiation was evaluated on the basis of HPRT mutant frequency and the micronucleus assay. A significant reduction in apoptotic cells was observed in cells incubated in modeled microgravity after gamma irradiation compared with cells maintained in 1g. Moreover, in irradiated cells, fewer G2-phase cells were found in modeled microgravity than in 1g, whereas more G1-phase cells were observed in modeled microgravity than in 1g. Genomic damage induced by ionizing radiation, i.e. frequency of HPRT mutants and micronucleated cells, increased more in cultures incubated in modeled microgravity than in 1g. Our results indicate that modeled microgravity incubation after irradiation affects cell response to ionizing radiation, reducing the level of radiation-induced apoptosis. As a consequence, modeled microgravity increases the frequency of damaged cells that survive after irradiation.

Apoptosis↗
PubMed1997

Increased sensitivity of scid heterozygous mice to ionizing radiation.

In the present study, acute effects of ionizing radiation on animal survival, bone marrow cells and fibroblast cell lines of scid homozygous, scid heterozygous and wild-type mice with the same C.B-17 genetic background were examined. The sensitivities to ultraviolet light (UV) and various chemicals, bleomycin, mitomycin C, N-methyl-N'-nitro-N-nitrosoguanidine, methyl methanosulphonate, 5-fluorouracil, 6-mercaptopurine, 4-nitroquinoline 1-oxide and potassium bromate) were also investigated. In addition, micronucleus testing of whole-body irradiated mice was performed. Scid heterozygous mice were found to be less sensitive than the homozygotes but more sensitive to ionizing radiation than wild-type mice, not only in vivo but also for bone marrow cells in vitro, suggesting partial dominance under both conditions. In contrast, there were no differences in sensitivity to UV light and various chemicals, as compared with wild-type and scid heterozygous cell lines, either in vitro or in the micronucleus test.

Animals↗
PubMedDate not supplied

[The effect of ionizing radiation on human muscle tissue].

The effect of ionizing radiation (gamma-irradiation of 60Co, doses from 10 Gy to 15 kGy) on human muscle tissue was studied using a biopsy material. Destructive alterations in muscle proteins were observed beginning from the dose of 1.0 kGy: appearance of new protein fractions with molecular mass 68-160 kDa and 18-36 kDa. Resistance of muscle proteins to the trypsin effect was unaltered, while the rate of pronase-induced hydrolysis was slightly increased, about 1.2-fold. Content of water and biomechanical properties of the tissue were unaltered, but the modulus of elasticity was decreased approximately 3-fold after treatment with maximal doses of the ionizing radiation used.

Adult↗
PubMed2000

Late effects of ionizing radiation on the microvascular networks in normal tissue.

Damage to the microvascular networks constitutes one of the most important components of ionizing radiation damage to normal tissue. Previously, we have reported the early (3, 7 and 30 days postirradiation) effects of ionizing radiation on the structure and function of normal tissue microvascular networks. Here we report on the late effects of ionizing radiation on the structural and functional changes in microvascular networks in locally irradiated (single 10-Gy dose) hamster cremaster muscles observed 60, 120 and 180 days postirradiation; age-matched animals were used as controls. As in the previous study, intravital microscopy was used to measure structural and functional parameters in complete microvascular networks in vivo. A factorial design was used to examine the effects of radiation status, time postirradiation, and network vessel type on the structure and function of microvascular networks. Our results indicate that the progression of radiation-induced microvascular damage continues during the late times but that there is partial recovery from radiation damage within 6 months postirradiation. Red blood cell flux, red blood cell velocity, and capillary blood flow in irradiated networks at 180 days postirradiation were significantly greater than control levels. As at the early times, all vessel types were not damaged equally by radiation at every time.

Animals↗
PubMed2005

Sensitivity of planktonic and biofilm-associated Salmonella spp. to ionizing radiation.

Salmonella enterica forms biofilms that are relatively resistant to chemical sanitizing treatments. Ionizing radiation has been used to inactivate Salmonella on a variety of foods and contact surfaces, but the relative efficacy of the process against biofilm-associated cells versus free-living planktonic cells is not well documented. The radiation sensitivity of planktonic or biofilm-associated cells was determined for three food-borne-illness-associated isolates of Salmonella. Biofilms were formed on sterile glass slides in a coincubation apparatus, using inoculated tryptic soy broth, incubated at 37 degrees C for 48 h. Resulting biofilms were 18 to 24 microm in height as determined by confocal scanning laser microscopy. The planktonic and biofilm cultures were gamma irradiated to doses of 0.0 (control), 0.5, 1.0, 1.5, 2.0 and 2.5 kGy. The D(10) value (the dose of radiation required to reduce a population by 1 log(10), or 90%) was calculated for each isolate-culture based on surviving populations at each radiation dose. The D(10) values of S. enterica serovar Anatum were not significantly (P < 0.05) different for biofilm-associated (0.645 kGy) and planktonic (0.677 kGy) cells. In contrast, the biofilm-associated cells of S. enterica serovar Stanley were significantly more sensitive to ionizing radiation than the respective planktonic cells, with D(10) values of 0.531 and 0.591 kGy, respectively. D(10) values of S. enterica serovar Enteritidis were similarly reduced for biofilm-associated (0.436 kGy) versus planktonic (0.535 kGy) cells. The antimicrobial efficacy of ionizing radiation is therefore preserved or enhanced in treatment of biofilm-associated bacteria.

Biofilms↗