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PubMed1997

Ionizing radiation-inducible apoptosis in the absence of p53 linked to transcription factor EGR-1.

The tumor suppressor protein p53 is a pivotal regulator of apoptosis, and prostate cancer cells that lack p53 protein are moderately resistant to apoptotic death by ionizing radiation. Genes encoding the transcription factor early growth response-1 (EGR-1) and cytokine tumor necrosis factor-alpha (TNF-alpha) were induced upon irradiation of prostate cancer cells, and inhibition of EGR-1 function resulted in abrogation of both TNF-alpha induction and apoptosis. Induction of the TNF-alpha gene by ionizing radiation and EGR-1 was mediated via a GC-rich EGR-1-binding motif in the TNF-alpha promoter. Because TNF-alpha induces apoptosis in prostate cancer cells, these findings suggest that, in the absence of p53, ionizing radiation-inducible apoptosis is mediated by EGR-1 via TNF-alpha transactivation.

Apoptosis↗
PubMed2001

Dephosphorylation and subcellular compartment change of the mitotic Bloom's syndrome DNA helicase in response to ionizing radiation.

Bloom's syndrome is a rare human autosomal recessive disorder that combines a marked genetic instability and an increased risk of developing all types of cancers and which results from mutations in both copies of the BLM gene encoding a RecQ 3'-5' DNA helicase. We recently showed that BLM is phosphorylated and excluded from the nuclear matrix during mitosis. We now show that the phosphorylated mitotic BLM protein is associated with a 3'-5' DNA helicase activity and interacts with topoisomerase III alpha. We demonstrate that in mitosis-arrested cells, ionizing radiation and roscovitine treatment both result in the reversion of BLM phosphorylation, suggesting that BLM could be dephosphorylated through the inhibition of cdc2 kinase. This was supported further by our data showing that cdc2 kinase activity is inhibited in gamma-irradiated mitotic cells. Finally we show that after ionizing radiation, BLM is not involved in the establishment of the mitotic DNA damage checkpoint but is subjected to a subcellular compartment change. These findings lead us to propose that BLM may be phosphorylated during mitosis, probably through the cdc2 pathway, to form a pool of rapidly available active protein. Inhibition of cdc2 kinase after ionizing radiation would lead to BLM dephosphorylation and possibly to BLM recruitment to some specific sites for repair.

Adenosine Triphosphatases↗
PubMed2002

The human organic cation transporter (hOCT2) recognizes the degree of substrate ionization.

The organic cation transporter, OCT2, plays a role in renal secretion of a broad array of weak bases. To determine whether the degree of ionization of these compounds plays a role in their interaction with OCT2, we examined the influence of external pH values on the activity of the human ortholog of OCT2, as expressed in Chinese hamster ovary-K1 cells. Importantly, changing the pH value from 7.0 to 8.0 had no effect on the rate of transport of the fixed cations, tetraethylammonium and 1-methyl-4-phenylpyridinium, i.e. the pH value did not have an effect upon the transporter itself. Cimetidine (pK(a) 6.92), a competitive inhibitor of hOCT2, displayed a 3.5-fold increase in IC(50) as pH values increased from 7 to 8. hOCT2-mediated cimetidine transport decreased over this pH range, the consequence of an increase in K(t) and decrease in J(max) at the higher pH value. The weak bases trimethoprim and 4-phenylpyridine showed a similar pattern of pH-sensitive interaction with hOCT2. The non-ionizable sterol, corticosterone, also inhibited hOCT2 activity, although it was neither competitive in nature nor was it sensitive to pH in the manner observed with weak bases. We conclude that the degree of ionization plays a critical role in binding of substrate to organic cation transporters.

Animals↗
PubMed1993

Ion effects in measurement of sodium and ionized calcium in direct potentiometry.

In some instruments that measure sodium directly in whole blood, plasma, or serum using ion selective electrodes (direct potentiometry), the higher the ionic strength of the solution, the lower is the sodium recovery in serum, as predicted by theory. The same could be expected for ionized calcium. When measuring the recovery of serum sodium on indirect potentiometric instrument and by flame photometry, which determine concentration in prediluted samples, and on direct potentiometric instruments, we observed that two out of the three direct potentiometry instruments showed a decreased recovery of sodium, as the ionic strength was increased, while on all the other instruments the recovery was complete. No effect of increased ionic strength was noted on the ionized calcium measurements in serum on all the instruments tested. Analysing pure aqueous solutions of sodium and calcium chloride with increased ionic strength on the same instruments, the sodium recovery was always complete or positive, and the same was true for ionized calcium. We postulate some effect of ionic strength on the salt bridge of the measuring systems, which is different when analysing serum or pure aqueous solutions.

Calcium↗
PubMed1994

Comparative effects of a Mg-enriched diet and different orally administered magnesium oxide preparations on ionized Mg, Mg metabolism and electrolytes in serum of human volunteers.

OBJECTIVE: To determine whether: 1) short-term dietary elevation in magnesium (Mg) intake could alter serum ionized Mg (IMg2+), total Mg (TMg); % ionized Mg (% IMg2+) and other cations; and 2) different formulated preparations of Mg oxide (MgO) in the presence and absence of phosphate could alter serum IMg2+, TMg, % IMg2+ and other cations in Mg-loaded subjects. METHODS: A randomized, triple cross-over study was performed on a rigorously defined group of normal male volunteers. Eighteen males were administered diets containing four to five times the United States recommended daily allowance (USRDA) of Mg followed by a randomization of three different MgO preparations, in the presence or absence of phosphate, containing equimolar amounts (12.34 mmol) of elemental Mg. Forty age-matched volunteers served as reference range controls. Specific ion selective electrodes were utilized to measure IMg2+, ionized calcium (ICa2+), sodium (Na+) potassium (K+) and hydrogen ion concentration (H+). Measurement of urinary excretion of Mg as well as TMg were determined by atomic absorption spectroscopy. RESULTS: Diets enriched with different oral formulations of Mg given for 6 days result in significant elevations in serum IMg2+ and % IMg2+ but not TMg, ICa2+, K+ or H+ in normal subjects. Although such Mg-loaded subjects demonstrate significant elevation in urinary excretion of Mg, no further changes in IMg2+, TMg or any of the serum cations were produced by ingestion of either of the three MgO preparations. Subjects showing normally low basal levels of serum IMg2+, (< or = 0.54 mM/L), could easily have their serum IMg2+ level manipulated by diets enriched with Mg, whereas subjects having average normal or high normal IMg2+ levels did not have their IMg2+ elevated significantly with either diets enriched with Mg or with exogenous MgO. CONCLUSION: These results indicate that since serum IMg2+ and % IMg2+, but not TMg, can be altered by dietary intake, previous or future findings which may indicate no change in TMg by diet may not reflect changes in biologically-active Mg.

Adolescent↗
PubMed1999

Prenatal exposure to ionizing radiation: sources, effects and regulatory aspects.

Knowledge and awareness of physicians and the general public concerning the risks of prenatal exposure to ionizing radiation are important when developing a correct attitude to ionizing radiation. This is particularly important in the justification of medical diagnostic exposure of pregnant women and in case of possible accidents. The present paper reviews the most recent data on the effects of prenatal exposure to ionizing radiation reported in the scientific literature and in documents of international organizations dealing with this subject. Potentially significant exposure for women of childbearing age in medical diagnostics, working conditions and environmental contamination following the Chernobyl accident are reported. Some examples of doses associated with medical exposure in the course of diagnostic examinations with X-rays and radiopharmaceuticals, and occupational exposure in workplaces are given. Lastly, the regulatory aspects of the European Union directives and the Italian legislation on medical and occupational exposure of women during pregnancy or in reproductive age are reviewed.

Dose-Response Relationship, Radiation↗
PubMed2000

Metallothionein induction in human CNS in vitro: neuroprotection from ionizing radiation.

PURPOSE: There have been extensive studies on the regulation of metallothionein (MT) synthesis, and its biological role in liver and kidney. Although there are few reports on brain MT, there is a growing interest in the role of MT in brain. There have been no publications to date on MT synthesis in the human central nervous system (CNS) following exposure to ionizing radiation. In the present study, primary human CNS cultures were used to examine the effect of ionizing radiation on MT mRNA and protein synthesis. In the same cultures, the neuroprotective effects of zinc (Zn) and cadmium (Cd)-induced MT synthesis from high-dose radiation were also examined. MATERIALS AND METHODS: Primary, serum-free, human CNS cultures were exposed to 30 or 60 Gy gamma-rays. The total MT protein was then measured by a Cd-heme assay, and mRNA for MT-II and MT-III was detected by reverse transcription polymerase chain reaction (RT-PCR). Cytotoxicity was measured by LDH release and apoptotic cell death by DNA fragmentation analysis. Sublethal neuroglial injury was assessed morphologically using specific astrocytic (glial fibrillary acidic protein--GFAP) and neuronal (microtubule-associated protein 2--MAP2) immunohistochemical markers. RESULTS: The total MT protein content was increased 12h after exposure to 30Gy. The increase in MT content in response to 60Gy was not statistically significant. MT-II mRNA levels increased at 3 and 6h after exposure to 30Gy gamma-rays, with a maximum expression at 12-24 h. MT-III mRNA was not significantly affected. Exposure to 60 Gy, but not 30 Gy, caused a marked increase in LDH release. Cells exposed to 30 Gy or less showed some apoptotic cell death by DNA fragmentation analysis, while exposure to 60 Gy resulted in a DNA smear confirmed by LDH assays. Preinduction of MT by 5 microM Cd or 100 microM Zn resulted in a significant reduction in radiation-induced LDH release. Morphological evaluations revealed that Cd or Zn preincubation led to relative preservation of MAP2 staining and GFAP. CONCLUSION: Both MT protein and MT-II mRNA can be induced in human CNS cells by ionizing radiation. Furthermore, induction of MT synthesis with Zn and Cd can protect human CNS cells from radiation-induced cytocidal and sublethal injuries. Both findings have implications in the development of strategies to protect human CNS tissue from damage during radiotherapy.

Brain↗
PubMed2001

MAPK dependence of DNA damage repair: ionizing radiation and the induction of expression of the DNA repair genes XRCC1 and ERCC1 in DU145 human prostate carcinoma cells in a MEK1/2 dependent fashion.

PURPOSE: To examine the role of mitogen-activated protein kinase (MAPK) signalling on the induction by ionizing radiation of the nucleotide excision repair gene (ERCC1), the X-ray cross-complementing group 1 protein (XRCC1) and the repair of radiation-induced DNA damage. MATERIALS AND METHODS: The expression of ERCC1 and XRCC1 was examined in DU145 human prostate cancer cells following exposure to ionizing radiation. We characterized the MAPK dependence of this expression through RT-PCR analysis, Western analysis, transcription inhibition and measurement of the activation of each promoter. Pre-exposure with the specific MEK1/2 inhibitor PD980059 (10 microM) was used to blunt radiation induction of MAPK without suppressing basal levels of MAPK activity. In addition, we examined the MAPK dependence of DNA damage repair by measuring radiation-induced micronucleus formation and the removal of and nicking activity associated with AP sites. RESULTS: Irradiation caused a time-dependent, MAPK-dependent increase in the protein levels of both ERCC1 and XRCC1. For each gene product, the protein level increase followed an increase in mRNA, which also was MAPK-dependent. Radiation also enhanced the activities of the ERCC1 and XRCC1 promoters in an MAPK-dependent fashion. Inhibition of transcription by DRB abolished the radiation-induced increase of ERCC1 and XRCC1 proteins. Inhibition of radiation-induced MAPK also diminished the ability of DU145 cells to remove AP sites and increased the number of cells displaying micronuclei following radiation exposure. CONCLUSIONS: These findings demonstrate a role for radiation-induced MAPK signalling in the regulation of DNA repair enzyme levels and DNA repair. Radiation-induced protein expression of ERCC1 and XRCC1 appears to require de novo transcription. These data suggest a significant role for MAPK signalling in the early response to DNA damage caused by ionizing radiation.

DNA Damage↗
PubMed2002

Protein kinase inhibitors modulate time-dependent effects of UV and ionizing irradiation on ICAM-1 expression on human hepatoma cells.

PURPOSE: To investigate modulation of the expression of the adhesion protein ICAM-1 by UV and ionizing irradiation. MATERIALS AND METHODS: HepG2 hepatoma cells were irradiated in vitro with UVB (20 mJ cm(-2)) or X-rays (5 Gy), respectively. Gene expression of ICAM-1 after irradiation was quantified by RT-PCR. Cell surface density of ICAM-1 was determined by flow cytometry. Protein or lipid kinase inhibitors were used to clarify radiation-induced transduction pathways that control ICAM-1 expression. Immuno-electron microscopy and dot-blot analysis were used to examine localization of ICAM-1. RESULTS: The study showed time-dependent effects of ionizing and UV irradiation on ICAM-1 expression of HepG2 cells. After an immediate transient decrease of ICAM-1 cell surface expression within minutes to hours, ICAM-1 expression increased up to 1.35-fold over normal level at 48 h post-irradiation. Irradiation caused ICAM-1 to become internalized into lysosomes. Additionally, ICAM-1 together with parts of the cell were pinched off. Finally, ICAM-1 levels were down- and up-regulated by decreased or increased gene expression. The early decrease of ICAM-1 expression could be blocked by a potent PKC inhibitor (BisX), whereas the increase of ICAM-1 after 24 h was prevented by addition of the p38 MAP kinase inhibitor SB 203580. CONCLUSION: The data suggest that ICAM-1 expression is modulated by UV, as well as ionizing radiation, in a time-dependent way involving PKC and p38 MAP kinase pathways.

Carcinoma, Hepatocellular↗
PubMed2002

Response of mammalian cell lines that undergo necrosis after ionizing irradiation to DNA-incorporated tritium and iodine-125 decays: implications for models of radiation action.

PURPOSE: To test the validity of enzymatic DNA repair-based models of ionizing radiation-induced mammalian cell killing. MATERIALS AND METHODS: Sensitivity to ionizing radiation-induced killing was determined by clonogenic survival assay. RESULTS: A panel of seven cell lines that have apparently normal enzymatic DNA repair capability and die predominantly by necrosis were shown to have marked differences in their sensitivity to killing by gamma- or X-irradiation. Despite such differences, the pseudo-diploid cell lines CHO, V79, and Vero (when corrected for differences in cell cycle distribution) and normal mouse embryo fibroblasts all had comparable D(o) values for killing by DNA-incorporated (125)I that were in the range of 57-66 decays; whilst the near-tetraploid or-triploid B16-F1, RUC-2 and SQ-20B cell lines had D(o) values of around 130 (125)I decays. The sensitivity of these cell lines to killing by DNA-incorporated (3)H decays was similarly related to ploidy. CONCLUSIONS: Differences in sensitivity to killing by DNA-incorporated (3)H or (125)I decays between the cell lines tested were primarily related to differences in ploidy and, second, to differences in cell cycle distribution or nuclear volume. The data do not support suggestions that generalized variability in an hypothetical aspect of enzymatic DNA repair can explain differences in sensitivity to killing by external-beam, low-linear energy transfer ionizing radiation.

Animals↗
PubMed2002

Transcription-based model for the induction of interchromosomal exchange events by ionizing irradiation in mammalian cell lines that undergo necrosis.

PURPOSE: To develop a model of the molecular events leading to ionizing radiation-induced interchromosomal exchange in mammalian cells that undergo necrosis. OUTLINE OF THE MODEL: DNA double-strand breaks (DSB), primarily those involving multiple individual damage sites (i.e. complex DSB), are postulated to be the critical initiating lesion. Only those DSB occurring in transcription units that are associated with transcription factories are postulated to induce chromosomal exchange events. It is suggested that such DSB are brought into contact with a DNA topoisomerase I (topo I) molecule through RNA polymerase II (pol II)-catalysed transcription and give rise to trapped DNA-topo I cleavage complexes. Trapped complexes are postulated to interact with another topo I molecule on a temporarily inactive transcription unit at the same transcription factory leading to DNA cleavage and subsequent strand exchange between the cleavage complexes. Interchromosomal exchange events will occur when the cleavage complexes are on transcription units located on different chromosomes. OUTCOMES: The model can explain a variety of phenomena that includes: the increased resistance to killing by ionizing radiation shown by quiescent cells (i.e. potentially lethal damage repair); the effect of ploidy on sensitivity to killing by DSB; the effect of chasing time on sensitivity to killing by DNA-incorporated (125)I decays after pulse labelling; and the size of the target for ionizing radiation-induced cell killing.

Animals↗
PubMed2005

p53-Dependent accelerated senescence induced by ionizing radiation in breast tumour cells.

Ionizing radiation has been reported to promote accelerated or premature senescence in both normal and tumour cell lines. The current studies were designed to characterize the accelerated senescence response to radiation in the breast tumour cell in terms of its dependence on functional p53 and its relationship to telomerase activity, telomere lengths, expression of human telomerase reverse transcriptase (hTERT, the catalytic subunit of telomerase) and human telomerase RNA (hTR, the RNA subunit of telomerase), as well as the induction of cytogenetic aberrations. Studies were performed in p53 wild-type MCF-7 cells, MCF-7/E6 cells with attenuated p53 function, MDA-MB231 cells with mutant p53 and MCF-7/hTERT cells with constitutive expression of hTERT. Telomerase activity was measured by the telomeric repeat amplification protocol (TRAP assay), telomere lengths by the terminal restriction fragment (TRF) assay, hTR and hTERT expression by reverse transcriptase-polymerase chain reaction (RT-PCR), senescence by beta-galactosidase staining, and apoptosis by TdT-mediated d-UTP-X nick-end labelling (TUNEL assay). Widespread and extensive expression of beta-galactosidase, a marker of cellular senescence, was evident in MCF-7 breast tumour cells following exposure to 10 Gy of ionizing radiation. Radiation did not suppress expression of either hTERT or hTR, alter telomerase activity or induce telomere shortening. Senescence arrest was also observed in irradiated MCF-7/hTERT cells, which have elongated telomeres due to the ectopic expression of the catalytic component of telomerase. In contrast to MCF-7 cells, irradiated MDA-MB231 breast tumour cells and MCF-7/E6 cells failed to senesce and instead demonstrated a delayed apoptotic cell death. Irradiation produced chromosome end associated abnormalities, including end-to-end fusions (an indicator of telomere dysfunction) in MCF-7 cells, MCF-7/hTERT cells, as well as in MCF-7/E6 cells. When cells were maintained in culture following irradiation, proliferative recovery was evident exclusively after senescence while the cell lines which responded to radiation by apoptosis continued to decline in cell number. Accelerated senescence in response to ionizing radiation is p53 dependent and associated with telomer dysfunction but is unrelated to changes in telomerase activity or telomere lengths, expression of hTERT and hTR. In the absence of functional p53, cells are unable to arrest for an extended period, resulting in apoptotic cell death while accelerated senescence in cells expressing p53 is succeeded by proliferative recovery.

Apoptosis↗
PubMed1980

The value of the photoreactivable component in E. coli Bs-1 cells exposed to densely and sparsely ionizing radiations.

The dependence of the photoreactivation effect in E. coli Bs-1 cells on LET and energy of sparsely ionizing radiation was studied. The photoreactivation was shown to be absent after densely ionizing radiation (alpha-particles of 239Pu; fast neutrons En = 0.85 MeV) and after sparsely ionizing radiation with energies below 200 keV. In those cases where photoreactivation took place, the photoreactivable sector was found to increase with the voltage of the radiation.

Alpha Particles↗
PubMed1988

Effects of ionizing radiation on the metabolism and longitudinal growth of cartilaginous embryonic chick tibiae in vitro.

The effect of ionizing radiation on the metabolism and longitudinal growth of cartilaginous tibiae of 6.5-day-old chick embryos was studied in vitro over a 3-day period. Before being cultured, tibiae received absorbed doses of 2 to 200 Gy. Of each pair, the counterpart served as control. Compared to the strong inhibition of [3H]thymidine incorporation, already 50 percent at 10 Gy, the effects of ionizing radiation on [3H]uridine and [3H]proline incorporation were limited: 20 and 40 percent respectively at 150 Gy. Metabolism of the cartilage cells in our organ culture was almost completely arrested at 200 Gy. Light and electron microscopy showed no morphological differences between irradiated and sham-irradiated tibiae until 150 Gy. At 200 Gy necrosis of most of the cells was observed. No differences in form and arrangement of extracellular fibers were noticed. The results of the metabolic studies and the morphological observations were correlated with the effects of ionizing radiation on the longitudinal growth. In contrast to DNA synthesis, RNA transcription and synthesis of collagen fibres were radioresistant processes.

Animals↗
PubMed1992

Membrane oxidative damage induced by ionizing radiation detected by diphenylhexatriene fluorescence lifetime distributions.

The sensitivity of the fluorescence lifetime of 1,6-diphenyl- 1,3,5-hexatriene (DPH) to the dielectric constant of its environment has been used to detect oxidative damage to phospholipid membranes induced by ionizing radiation. The DPH fluorescence decay in phospholipid vesicles is described well by a continuous distribution of lifetime values, reflecting the various DPH depths in the bilayer and related to the gradient of the dielectric constant. Ionizing radiation oxidizes unsaturated acyl residues of phospholipids, altering the dielectric constant across the bilayer, sharpening the distribution of DPH lifetimes and increasing the centre of the distribution. Ionizing radiation doses between 22 and 110 Gy were used, and were effective only in the presence of oxygen. A model based on the formation of packing defects in the bilayer describes the phenomenon.

Diphenylhexatriene↗
PubMed1994

Initial events in the cellular effects of ionizing radiations: clustered damage in DNA.

General correlations are found between the detailed spatial and temporal nature of the initial physical features of radiation insult and the likelihood of final biological consequences. These persist despite the chain of physical, chemical and biological processes that eliminate the vast majority of the early damage. Details of the initial conditions should provide guidance to critical features of the most relevant early biological damage and subsequent repair. Ionizing radiations produce many hundreds of different simple chemical products in DNA and also multitudes of possible clustered combinations. The simple products, including single-strand breaks, tend to correlate poorly with biological effectiveness. Even for initial double-strand breaks, as a broad class, there is apparently little or no increase in yield with increasing ionization density, in contrast with the large rise in relative biological effectiveness for cellular effects. Track structure analysis has revealed that clustered DNA damage of severity greater than simple double-strand breaks is likely to occur at biologically relevant frequencies with all ionizing radiations. Studies are in progress to describe in more detail the chemical nature of these clustered lesions and to consider the implications for cellular repair. It has been hypothesized that there is reduced repair of the more severe examples and that the spectrum of lesions that dominate the final cellular consequences is heavily skewed towards the more severe, clustered components.

Animals↗
PubMed1994

Possible role of inner-shell ionization phenomena in cell inactivation by heavy ions.

The existence of a correlation between experimental probabilities of cell inactivation by charged particles and calculated probabilities for K-vacancy production in heavy atoms (C, N, O, P) of the DNA of cell nuclei is established. Both phenomena display a similar dependence upon the linear energy transfer (LET) of incident particles. In particular for low LET values, K cross sections for various incident ions have nearly the same functional dependence on ion-LET and for higher LET-values, K cross sections display maxima which look like those of inactivation cross sections. These characteristics are well-understood features of the K-ionization phenomenon, in particular the maxima of probability occur for projectile velocities near orbital velocities of the ejected electrons. The meaning of the observed correlation is discussed in terms of deposited energy and in the light of existing experimental results on cell inactivation by X-ray absorption at K-threshold. We consider a mechanism which has already been evoked to explain these photo-absorption experiments and which assumes that a K ionization triggers a double-strand break by Coulomb explosion and energy dissipation of Auger electrons. However, it is seen that K cross sections are important for C, N and O atoms but negligible for P atoms. Thus, the lesion considered here affects other atoms than those involved in the K-photoabsorption experiments. The lesion efficiency with respect to subsequent double-strand breakage and repair processes is not yet known, however one may suspect a direct link between DNA blunt ends possibly induced by such K ionizations and cell inactivation.

Animals↗
PubMed1996

Ionizing radiation modulates the spread of an apathogenic rabies virus in mouse brain.

Ionizing radiation has been shown to affect a broad range of viral diseases including neurotropic infections through an immunosuppression mechanism. In the present study we have investigated the effect of ionizing radiation on the characteristics of neurotropic infection by rabies virus, which has the unusual feature of infecting almost exclusively neurons. In order to analyze better the effect produced, the study concerned the spread of an apathogenic rabies virus variant in mouse brain. Irradiation was shown to increase both the intensity and duration of the infection in a reversible and dose-dependent manner and was effective in whole-body irradiation and in head-protected body irradiation, whereas cephalic irradiation had no effect. These results underline the role played by the immune system in the regulation of neurotropic virus infections in the brain and show that phenomena such as viral clearance and time-course of a neurotropic viral infection may be significantly modified by ionizing radiation, even for viruses whose infection involves only neurons.

Animals↗