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Results for “Radiation, Ionizing”

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PubMedDate not supplied

Cell-density dependent effects of low-dose ionizing radiation on E. coli cells.

The changes in genome conformational state (GCS) induced by low-dose ionizing radiation in E. coli cells were measured by the method of anomalous viscosity time dependence (AVTD) in cellular lysates. Effects of X-rays at doses 0.1 cGy--1 Gy depended on post-irradiation time. Significant relaxation of DNA loops followed by a decrease in AVTD. The time of maximum relaxation was between 5-80 min depending on the dose of irradiation. U-shaped dose response was observed with increase of AVTD in the range of 0.1-4 Gy and decrease in AVTD at higher doses. No such increase in AVTD was seen upon irradiation of cells at the beginning of cell lysis while the AVTD decrease was the same. Significant differences in the effects of X-rays and gamma-rays at the same doses were observed suggesting a strong dependence of low-dose effects on LET. Effects of 0.01 cGy gamma-rays were studied at different cell densities during irradiation. We show that the radiation-induced changes in GCS lasted longer at higher cell density as compared to lower cell density. Only small amount of cells were hit at this dose and the data suggest cell-to-cell communication in response to low-dose ionizing radiation. This prolonged effect was also observed when cells were irradiated at high cell density and diluted to low cell density immediately after irradiation. These data suggest that cell-to-cell communication occur during irradiation or within 3 min post-irradiation. The cell-density dependent response to low-dose ionizing radiation was compared with previously reported data on exposure of E. coli cells to electromagnetic fields of extremely low frequency and extremely high frequency (millimeter waves). The body of our data show that cells can communicate in response to electromagnetic fields and ionizing radiation, presumably by reemission of secondary photons in infrared-submillimeter frequency range.

Bacteriolysis↗

PubMed2005

Micronuclei in humans induced by exposure to low level of ionizing radiation: influence of polymorphisms in DNA repair genes.

Understanding the risks deriving from protracted exposure to low doses of ionizing radiation has remarkable societal importance in view of the large number of work settings in which sources of IR are encountered. To address this question, we studied the frequency of micronuclei (MN), which is an indicator of DNA damage, in a population exposed to low levels of ionizing radiation and in matched controls. In both exposed population and controls, the possible influence of single nucleotide polymorphisms in XRCC1, XRCC3 and XPD genes on the frequency of micronuclei was also evaluated. We also considered the effects of confounding factors, like smoking status, age and gender. The results indicated that MN frequency was significantly higher in the exposed workers than in the controls [8.62+/-2.80 versus 6.86+/-2.65; P=0.019]. Radiological workers with variant alleles for XRCC1 or XRCC3 polymorphisms or wild-type alleles for XPD exon 23 or 10 polymorphisms showed a significantly higher MN frequency than controls with the same genotypes. Smoking status did not affect micronuclei frequency either in exposed workers or controls, while age was associated with increased MN frequency in the exposed only. In the combined population, gender but not age exerted an influence on the yield of MN, being higher in females than in males. Even though there is a limitation in this study due to the small number of subjects, these results suggest that even exposures to low level of ionizing radiation could have genotoxic effects and that XRCC3, XRCC1 and XPD polymorphisms might contribute to the increased genetic damage in susceptible individuals occupationally exposed to chronic low levels of ionizing radiation. For a clear conclusion on the induction of DNA damage caused by protracted exposure to low doses of ionizing radiation and the possible influence of genetic polymorphism in DNA repair genes larger studies are needed.

Biomarkers↗

PubMed1992

Effects of ionizing radiation and beta-adrenergic stimulation on the expression of early response genes in rat parotid glands.

There is little known about the regulation of gene expression in rat parotid glands after exposure to ionizing radiation. The present studies investigate the effects of in vivo ionizing radiation, with subsequent stimulation of beta-adrenergic receptors by isoproterenol, on parotid gland function and on the expression of the early response genes, c-fos, c-jun, and jun B. Ionizing radiation diminished parotid gland weight and saliva output. Treatment of irradiated rats with isoproterenol increased the gland weight to levels similar to those in nonirradiated rats. However, such treatment had no effect on saliva output as indicated by measurements of parotid salivary flow rate. Irradiation alone increased the expression of c-fos, c-jun, and jun B. The combination of irradiation and isoproterenol had an additional effect on the levels of c-fos and jun B mRNAs and proteins particularly at earlier experimental times (1 to 8 h). Isoproterenol alone induced high levels of c-fos and jun B mRNA but not of c-jun mRNA. However, c-jun mRNA was induced markedly by radiation and 8 h of isoproterenol treatment, indicating a combined effect on c-jun gene expression. These observations suggest that the expression of the proto-oncogenes c-fos, c-jun, and jun B is probably regulated through differential signal transduction pathways which may be activated by these external stimuli and may be associated with functional changes induced in the rat parotid gland by ionizing radiation and by ionizing radiation and isoproterenol.

Animals↗

PubMed2004

Protective effects of melatonin on the ionizing radiation induced DNA damage in the rat brain.

Melatonin is an endogenously produced antioxidant with radioprotective actions while ionizing radiation is a well-known cytotoxic and mutagenic agent of which the biological results are attributable to its free radical producing effects. The effect of melatonin on the DNA strand breakage and lipid peroxidation induced by ionizing radiation in the rat brain were investigated in order to clarify its radioprotective ability. The DNA strand breakage in rat brain exposed to 1000 cGy ionizing radiation was assessed by alkaline single cell gel electrophoresis and the lipid peroxidation was evaluated by measuring thiobarbituric acid reactive substances (TBARS) concentrations. A significant increase in DNA damage (p < 0.05) and TBARS concentrations (p < 0.01) was found in the radiation treated rat brain. Pre-treatment of rats with intraperitoneal doses of 100 mg/kg melatonin provided a significant decrease in the DNA strand breakage and lipid peroxidation. Our results indicate that melatonin can protect brain cells from oxidative damage induced by ionizing radiation.

Animals↗

PubMed1992

Ionizing radiation stimulates unidentified tyrosine-specific protein kinases in human B-lymphocyte precursors, triggering apoptosis and clonogenic cell death.

Very little is known regarding the effects of ionizing radiation on cytoplasmic signal transduction pathways. Here, we show that ionizing radiation induces enhanced tyrosine phosphorylation of multiple substrates in human B-lymphocyte precursors. This response to ionizing radiation was also observed in cells pretreated with vanadate, a potent protein-tyrosine-phosphatase (PTPase) inhibitor, and phosphotyrosyl [Val5]angiotensin II phosphatase assays showed no decreased PTPase activity in irradiated cells. Thus, enhanced tyrosine phosphorylation in irradiated B-lymphocyte precursors is not triggered by inhibition of total cellular PTPase activity. Immune-complex kinase assays using anti-phosphotyrosine antibodies demonstrated enhanced protein-tyrosine kinase (PTK) activity in the immunoprecipitates from irradiated cells, and the PTK inhibitors genistein and herbimycin effectively prevented radiation-induced tyrosine phosphorylation. Immune-complex kinase assays on irradiated and unirradiated B-lymphocyte precursors using antibodies prepared against unique amino acid sequences of p59fyn, p56/p53lyn, p55blk, and p56lck demonstrated that these Src-family tyrosine kinases were not the primary PTKs responsible for enhanced tyrosine kinase activity in the anti-phosphotyrosine antibody immunoprecipitates or for enhanced tyrosine phosphorylation of multiple substrates. Thus, our findings favor the hypothesis that ionizing radiation induces enhanced tyrosine phosphorylation in B-lymphocyte precursors by stimulation of as yet unidentified PTKs. Tyrosine phosphorylation appears to be an important proximal step in radiation-induced apoptosis and clonogenic cell death because inhibition of PTK prevents DNA fragmentation and loss of clonogenicity of irradiated B-lymphocyte precursors. Since PTKs play myriad roles in the regulation of cell function and proliferation, the activation of a PTK cascade, as detailed in this report, may explain some of the pleiotropic effects of ionizing radiation on cellular functions of B-lymphocytes and their precursors.

Apoptosis↗

PubMed2004

[Combined effects of endostatin gene transfer and ionizing radiation on lung adenocarcinoma model of A549-cells].

OBJECTIVE: The combined inhibition effects of endostatin gene transfer and ionizing radiation on lung adenocarcinoma model of A549-cell were investigated. METHODS: Human endostatin gene was transferred into lung adenocarcinoma A549 cell by retrovirus-mediation to obtain an A549/Endo cell. A549 and A549/Endo cells were xenoimplanted in nude mice respectively (each group included 10 mice). Then, the changes of the tumor size of each group (n = 5) and its growth inhibition rate were estimated. The implanted tumors of each group (n = 5) were exposed to radiation with 20 Gy at 28 day after implantation. They were irradiated again with 20 Gy 3 day later. The ionizing radiation was strictly confined to the tumor by shielding the rest of the body with lead. The size of tumor was measured periodically. The microvessel density (MVD) of 4 groups of implanted tumors (A549, A549/Endo, A549 + IR and A549/Endo + IR) were compared on day 42 postgrafting by the immunohistochemical method. RESULTS: PCR confirmed that endostatin gene was inserted into the genomic DNA of human lung adenocarcinoma A549 cell. The tumor formation time showed significant difference (P < 0.05) between group A549 (7.8 +/- 1.6) d and group A549/Endo (12.2 +/- 1.7) d. At the time of day 42 postgrafting, the tumor sizes of group A549 and group A549/Endo were (927.8 +/- 269.2) mm3 and (217.5 +/- 81.5) mm3 respectively (P < 0.01), and the tumor growth inhibition rate was 76. 5%. At the time of day 14 after irradiation, the tumor sizes of group A549 and group A549/Endo were (157.7 +/- 49.0) mm3 and (4.6 +/- 2.9) mm3 respectively (P < 0.01). The results of immunohistochemical detection showed that the MVD of-A549/Endo implanted tumor was significantly decreased [21.62 +/- 3.55 compared with A549 implanted tumor 35.78 +/- 5.67 (P < 0.01)]. Moreover , it also showed that ionizing radiation could further reduce the MVD of A549/Endo implanted tumor from 21.62 +/- 3.55 to 11.32 +/- 2.78 (P < 0.01). CONCLUSIONS: Retroviruses can highly mediate the transfer of endostatin gene into the adenocarcinoma cells. Endostatin gene transfer can inhibit the xenoimplanted tumor growth by its direct inhibition on neovascularization. The combination of endostatin gene transfer with ionizing radiation treatment can synergistically inhibit the neovascularization and the growth of lung adenocarcinoma.

Adenocarcinoma↗

PubMed2002

The use of a genetically engineered herpes simplex virus (R7020) with ionizing radiation for experimental hepatoma.

The herpes simplex virus (HSV) recombinant virus R7020 is an attenuated virus designed as a candidate for immunization against both HSV-1 and HSV-2 infections. It was extensively tested in an experimental animal system and in a healthy human adult population without significant untoward effects. We report on the use of R7020 with ionizing radiation as an oncolytic agent for hepatomas. Two hepatoma cell lines were studied, Hep3B and Huh7. R7020 replicated to higher titers in Hep3B cells than in Huh7 cells. Tissue culture studies correlated with hepatoma xenograft responses to R7020. R7020 was more effective in mediating Hep3B tumor xenograft regression compared with Huh7. Ionizing radiation combined with R7020 also showed differential results in antitumor efficacy between the two cell lines in tumor xenografts. Ionizing radiation enhanced the replication of R7020 in Hep3B xenografts. Moreover, the combination of ionizing radiation and virus caused a greater regression of xenograft volume than either R7020 or radiation alone. Ionizing radiation had no effect on the replication of R7020 virus in Huh7 xenografts. These results indicate that a regimen involving infection with an appropriate herpesvirus such as R7020 in combination with ionizing radiation can be highly effective in eradicating certain tumor xenografts.

Animals↗

PubMed2006

Hypothetical HTLV-I induction by ionizing radiation.

Some laboratories have reported HTLV-I genome integration in cancer patients diagnosed with neoplasms of cervix and uterus. Usually, cancer patients undergo radiotherapy besides chemotherapy and surgery. It is hypothesized that radiation exposure would induce HTLV-I genome generation/activation, nevertheless there is not any report on experimental procedures trying to demonstrate HTLV-I gene expression in cells exposed to ionizing radiation. Anyway, earlier experimental works by Lieberman and Kaplan in 1959 succeeded to isolate retroviral particles, the radiation leukemia virus (RadLV), from thymic lymphomas of X-ray-irradiated C57BL/Ka mice, assuming that RadLV activated in the host by ionizing radiation, is released and transported to the thymus, where lymphoblasts, generated during the postradiation recovery phase, constitute an optimal target cell population for both replication of and eventual transformation by virus. Recent studies claim that besides RadLV, another retrovirus (RadLV-0) also induced by ionizing radiation is expressed and would be responsible for transformed cells of bone marrow origin. Epidemiological studies coincidentally point out to high incidence of HTLV-I infection in geographic areas displaying significant levels of radioactivity contamination as in Central Africa, Japan Islands and Mururoa Atoll. In our research work, we detected HTLV-I antibodies and viral genome integration in cancer patients of cervix and uterus and health care workers, whose had been exposed to ionizing radiation during radiotherapeutic procedures. Recombinational events among endogenous retrovirus and other retrogenic elements in the host cell genome under the bombardment of ionizing radiation from different sources could have optimized the phenomena occurrence or even ignited them to happen, generating HTLV-I genome, related viral peptides and virions. Therefore, it is feasible that exposure to ionizing radiation during therapeutic procedures could generate HTLV-I genome or induce the virus to be expressed in cells of cancer patients submitted to radiotherapy as also in healthy subjects under the same conditions, in artificial or natural radiation environment.

Animals↗

PubMed2000

Magnetic resonance imaging (MRI) controlled outcome of side effects caused by ionizing radiation, treated with 780 nm-diode laser -- preliminary results.

BACKGROUND AND OBJECTIVE: Ionizing radiation therapy by way of various beams such as electron, photon and neutron is an established method in tumor treatment. The side effects caused by this treatment such as ulcer, painful mastitis and delay of wound healing are well known, too. Biomodulation by low level laser therapy (LLLT) has become popular as a therapeutic modality for the acceleration of wound healing and the treatment of inflammation. Evidence for this kind of application, however, is not fully understood yet. This study intends to demonstrate the response of biomodulative laser treatment on the side effects caused by ionizing radiation by means of magnetic resonance imaging (MRI). STUDY DESIGN/PATIENTS AND METHODS: Six female patients suffering from painful mastitis after breast ionizing irradiation and one man suffering from radiogenic ulcer were treated with lambda=780 nm diode laser irradiation at a fluence rate of 5 J/cm2. LLLT was performed for a period of 4-6 weeks (mean sessions: 25 per patient, range 19-35). The tissue response was determined by means of MRI after laser treatment in comparison to MRI prior to the beginning of the LLLT. RESULTS: All patients showed complete clinical remission. The time-dependent contrast enhancement curve obtained by the evaluation of MR images demonstrated a significant decrease of enhancement features typical for inflammation in the affected area. CONCLUSION: Biomodulation by LLLT seems to be a promising treatment modality for side effects induced by ionizing radiation.

Adult↗

PubMed1990

The skin: its structure and response to ionizing radiation.

The response of the skin to ionizing radiation has important implications both for the treatment of malignant disease by radiation and for radiological protection. The structural organization of human skin is described and compared with that of the pig, with which it shows many similarities, in order that the response of the skin to ionizing radiation may be more fully understood. Acute radiation damage to the skin is primarily a consequence of changes in the epidermis; the timing of the peak of the reaction is related to the kinetic organization of this layer. The rate of development of damage is independent of the radiation dose, since this is related to the natural rate of loss of cells from the basal layer of the epidermis. Recovery of the epidermis occurs as a result of the proliferation of surviving clonogenic basal cells from within the irradiated area. The presence of clonogenic cells in the canal of the hair follicle is important, particularly after non-uniform irradiation from intermediate energy beta-emitters. The migration of viable cells from the edges of the irradiated site is also significant when small areas of skin are irradiated. Late damage to the skin is primarily a function of radiation effects on the vasculature; this produces a wave of dermal atrophy after 16-26 weeks. Dermal necrosis develops at this time after high doses. A second phase of dermal thinning is seen to develop after greater than 52 weeks, and this later phase of damage is associated with the appearance of telangiectasia. Highly localized irradiation of the skin, either to a specific layer (as may result from exposure to very low energy beta-emitters) or after exposure to small highly radioactive particles, 'hot particles', produces gross effects that become visibly manifest within 2 weeks of exposure. These changes result from the direct killing of the cells of the skin in interphase after doses greater than 100 Gy. Dose-effect curves have been established for the majority of these deterministic endpoints in the skin from the results of both experimental and clinical studies. These are of value in the establishment of safe radiation dose limits for the skin.

Animals↗

PubMed1993

Coinduction of c-jun gene expression and internucleosomal DNA fragmentation by ionizing radiation.

Previous work has demonstrated that the cellular response to ionizing radiation includes transcriptional activation of the c-jun early response gene. The present studies demonstrate that this induction of c-jun expression is temporally related to the appearance of internucleosomal DNA fragmentation. These events were maximal at 6 h and transient after exposure to lethal doses (20 Gy) of ionizing radiation. We also demonstrate that N-acetyl-L-cysteine (NAC), an antioxidant, inhibits X-ray-induced c-jun expression and endonucleolytic DNA cleavage. These findings suggested that both events are mediated at least in part through the formation of reactive oxygen intermediates (ROIs). Since ROIs damage DNA and X-ray-induced DNA damage is associated with activation of poly(ADP-ribose) polymerase (ADPRP), we studied the effects of the ADPRP inhibitors 3-aminobenzamide (3-AB), nicotinamide, and theophylline. 3-AB blocked both X-ray-induced c-jun expression and internucleosomal DNA fragmentation. Similar findings were obtained with nicotinamide and theophylline. In contrast, 3-AB had little if any effect on induction of c-jun transcripts or DNA fragmentation induced by the alkylating agent mitomycin C. While c-jun expression is restricted to cells in G1 and G1/S phases, we have found that X-ray-induced c-jun transcripts are detectable throughout all phases of the cell cycle. The induction of internucleosomal DNA fragmentation by X-rays was also detectable throughout the cell cycle. Taken together, these results support the coinduction of c-jun transcription and internucleosomal DNA fragmentation by ionizing radiation. Similar studies were performed with H2O2 since this agent also results in the production of ROIs.(ABSTRACT TRUNCATED AT 250 WORDS)

Cell Line↗

PubMed1992

No adaptive response of Chinese hamster ovary cells to low doses of ionizing radiation.

Chinese hamster ovary (CHO) cells that had been exposed to very low doses of ionizing radiation from incorporated tritiated thymidine or X-rays were shown not to be more resistant to the induction of chromatid aberrations by a subsequent higher dose of ionizing radiation than previously untreated cells. The adaptive response to ionizing radiation was absent both in cells challenged with high doses of X-rays (1.25 Gy) and in cells post-treated with thermal neutrons (0.5-1 x 10(12) n/cm2). In agreement with these observations in CHO cells we were unable to demonstrate an adaptive response to X-rays also in human lymphocytes from five different donors.

Adaptation, Physiological↗

PubMed1977

[Radiation therapy in patients with electronic cardiac pacemakers: interferences with the pacemaker's function by ionizing radiation and other sources of disturbances (author's transl)].

In the course of radiation therapy and connected diagnostical measures ionizing radiation and other sources of disturbance may interfere with the function of permanent pacemakers. The conditions of such hazards are investigated in theory and practice making allowance for the different susceptibility to trouble of various models of permanent pacemakers. It appears that no extension of long-term follow-up of the cardiac pacemaker's function is needed with regard to possible late effects of ionizing radiation, but that the follow-up of pacemaker-patients during their first period of treatment should not be neglected, since other sources of electronic interference may be present. Routine checks as radiotherapy installations should also include possible sources of disturbance to electronic pacemakers.

Aged↗

PubMed1993

Synergistic effects of ionizing radiation and 60 Hz magnetic fields.

Experiments designed to evaluate the synergistic production of clastogenic effects by ionizing radiation and 60 Hz magnetic fields were performed using human lymphocytes from peripheral blood. Following exposure to ionizing radiation, cells were cultured in 60 Hz magnetic fields having field strengths up to 1.4 mT. Cells exposed to both ionizing radiation and 60 Hz magnetic fields demonstrated an enhanced frequency of near tetraploid chromosome complements, a feature not observed following exposure to only ionizing radiation. The results are discussed in the context of a multiple-stage model of cellular transformation, employing both initiating and promoting agents.

Electromagnetic Fields↗

PubMed1981

A study of the peroxidation of fatty acid micelles promoted by ionizing radiation, hydrogen peroxide and ascorbate.

the kinetics of peroxidation of fatty acid micelles promoted by ionizing radiation, hydrogen peroxide and ascorbate were compared. At the dose-rate range of ionizing radiation studied, the higher the dose-rate, the greater the total dose required to produce the same effect. With ascorbate, the rate of lipid peroxidation was dependent on the concentration of the promoter only up to 1 X 10(-4) M, beyond which a decreasing rate of peroxidation induction was observed. Higher concentration of ascorbate also suppressed the promoting effect of ionizing radiation. Formate, a hydroxyl radical scavenger, inhibited the peroxidation process promoted by these three agents. Caesium was found to be slightly inhibitory. EDTA and deoxycholate were also inhibitory, which may be attributed to iron-chelating and micelle-disrupting capacity, respectively. Addition of iron (Fe2+ or Fe3+) to EDTA-chelated fatty acid micelles re-initiated the peroxidation process. The ease of fatty acid oxidation at pH 7.5 was arochidonic (20:4) greater than linolenic (18:3) greater than linoleic (18:2). This order was reversed at pH 11.5. Similarities in the kinetics of peroxidation obtained suggest that certain biological sequelae encountered in cells treated with these seemingly dissimilar agents might arise through some common mechanism(s).

Ascorbic Acid↗

PubMedDate not supplied

Effect of ionizing radiation on partial seizures attributable to malignant cerebral tumors.

Empirical evidence in the clinical literature suggests that ionizing radiation influences human epileptic behavior. A group of patients with tumor-associated epilepsy, biopsy-proven malignancy, and primary antineoplastic treatment with ionizing radiation was selected to evaluate this observation. The antiepileptic effect of ionizing radiation was examined in 9 patients presenting with malignant cerebral tumor and medically refractory partial seizures during at least 2 months. Tissue diagnosis was obtained by stereotactic biopsy without further surgery. Histological categories included anaplastic astrocytoma (5 cases), glioblastoma (2), lymphoma (1), and metastatic non-small cell carcinoma of the lung (1). All patients had medically refractory simple partial seizures with or without secondary generalization with frequencies of 3/week to 8/day for 2-7 months before completion of therapy. Fractionated radiation therapy by parallel opposed fields was delivered with a cumulative dose range of 3,000-6,600 cGy. One patient also had 125I brachytherapy with implant removal after 6 months. Five patients had a seizure-free outcome for periods lasting 2-12 months, whereas the remainder experienced a reduction in frequency of greater than 75% during a follow-up period of 3 months to 6 years. One patient with a glioblastoma remained seizure-free for 3 months and experienced 2 generalized seizures during tumor progression and clinical deterioration but otherwise remained under good anticonvulsant control until his death after 1 year. This review of cases of partial seizures attributable to an unresected malignant cerebral tumor indicates that ionizing radiation may have a favorable effect upon medically refractory partial seizures with significant reduction or elimination of seizures. Moreover, the effect lasts beyond the immediate and early postradiation period. The therapy may thus also lessen the propensity for cerebral tissue towards later epileptogenicity that gives rise to a partial seizure disorder.

Adolescent↗

PubMed1999

The tyrosine kinase lck is required for CD95-independent caspase-8 activation and apoptosis in response to ionizing radiation.

Induction of apoptosis is a hallmark of cytostatic drug and radiation-induced cell death in human lymphocytes and lymphoma cells. However, the mechanisms leading to apoptosis are not well understood. We provide evidence that ionizing radiation induces a rapid activation of caspase-8 (FLICE) followed by apoptosis independently of CD95 ligand/receptor interaction. The radiation induced cleavage pattern of procaspase-8 into mature caspase-8 resembled that following CD95 crosslinking and resulted in cleavage of the proapoptotic substrate BID. Overexpression of dominant-negative caspase-8 interfered with radiation-induced apoptosis. Caspase-8 activation by ionizing radiation was not observed in cells genetically defective for the Src-like tyrosine kinase Lck. Cells lacking Lck also displayed a marked resistance towards apoptosis induction upon ionizing radiation. After retransfection of Lck, caspase-8 activation and the capability to undergo apoptosis in response to ionizing radiation was restored. We conclude that radiation activates caspase-8 via an Lck-controlled pathway independently of CD95 ligand expression. This is a novel signaling event required for radiation induced apoptosis in T lymphoma cells.

Antibodies↗

PubMed2003

The alkaline Comet assay as biomarker in assessment of DNA damage in medical personnel occupationally exposed to ionizing radiation.

The alkaline Comet assay was selected as a biomarker of exposure to evaluate the ongoing exposure to ionizing radiation of 50 medical workers occupationally exposed to ionizing radiation and 50 corresponding unexposed control subjects. The primary DNA damage was evaluated by measuring the extent of DNA migration in peripheral blood leukocytes. The inter-individual differences in DNA damage between exposed subjects were compared with their dosimeter readings and occupation. It was found that medical workers who were occupationally exposed to ionizing radiation for different periods of time showed highly significant increases in levels of DNA damage compared with controls. However, influences of the different occupational settings and doses absorbed on the levels of DNA damage, assessed by use of the Comet assay, might be excluded in the majority of subjects. Differences in comet parameters measured due to smoking and gender were not statistically significant in either exposed or control subjects. The results obtained have confirmed the usefulness of the alkaline Comet assay as an additional complement to standard biodosimetric methods. By detection of momentary DNA damage and/or repair activity, it reflects the concurrent exposure and the actual levels of DNA damage present in peripheral blood leukocytes of the radiological workers at the moment of blood sampling.

Biomarkers↗