UV-type damage associated with ionizing radiation: a review

The induction of UV-type damage by ionizing radiation in repair deficient strains of E. coli is reviewed. Both photoreactivable and non-photoreactivable types of damage can be observed. The induction of UV-type damage is largely independent of the presence of free-radical reactive agents (e.g. oxygen and thiols), but is dependent upon the energy of the photon--or electron--beam used, the radiation geometry and the optical absorbance of the extracellular medium. On the basis of calculations and experimental evidence, it is clear that one mechanism whereby such damage arises is through the generation of Cerenkov emission. However, small yields of UV-type damage can be produced using X-rays whose energy is below the threshold for production of Cerenkov emission. In this instance, the damage induction mechanism is thought to involve a direct excitation process.     

Untargeted effects of ionizing radiation: implications for radiation pathology

The dogma that genetic alterations are restricted to directly irradiated cells has been challenged by observations in which effects of ionizing radiation, characteristically associated with the consequences of energy deposition in the cell nucleus, arise in non-irradiated cells. These, so called, untargeted effects are demonstrated in cells that have received damaging signals produced by irradiated cells (radiation-induced bystander effects) or that are the descendants of irradiated cells (radiation-induced genomic instability). Radiation-induced genomic instability is characterized by a number of delayed adverse responses including chromosomal abnormalities, gene mutations and cell death. Similar effects, as well as responses that may be regarded as protective, have been attributed to bystander mechanisms. Whilst the majority of studies to date have used in vitro systems, some adverse non-targeted effects have been demonstrated in vivo. However, at least for haemopoietic tissues, radiation-induced genomic instability in vivo may not necessarily be a reflection of genomically unstable cells. Rather the damage may reflect responses to ongoing production of damaging signals; i.e. bystander responses, but not in the sense used to describe the rapidly induced effects resulting from direct interaction of irradiated and non-irradiated cells. The findings are consistent with a delayed and long-lived tissue reaction to radiation injury characteristic of an inflammatory response with the potential for persisting bystander-mediated damage. An important implication of the findings is that contrary to conventional radiobiological dogma and interpretation of epidemiologically-based risk estimates, ionizing radiation may contribute to malignancy and particularly childhood leukaemia by promoting initiated cells rather than being the initiating agent. Untargeted mechanisms may also contribute to other pathological consequences.     

Assessing the impact of ionizing radiation on aquatic invertebrates: a critical review

There is growing scientific, regulatory and public concern over anthropogenic input of radionuclides to the aquatic environment, especially given the issues surrounding existing nuclear waste, future energy demand and past or potential nuclear accidents. A change in the approach to how we protect the environment from ionizing radiation has also underlined the importance of assessing its impact on nonhuman biota. This review presents a thorough and critical examination of the available information on the effects of ionizing radiation on aquatic invertebrates, which constitute approximately 90% of extant life on the planet and play vital roles in ecosystem functioning. The aim of the review was to assess the progress made so far, addressing any concerns and identifying the knowledge gaps in the field. The critical analysis of the available information included determining yearly publications in the field, qualities of radiation used, group(s) of animals studied, and levels of biological organization at which effects were examined. The overwhelming conclusion from analysis of the available information is that more data are needed in almost every area. However, in light of the current priorities in human and environmental health, and considering regulatory developments, the following are areas of particular interest for future research on the effects of ionizing radiation on nonhuman biota in general and aquatic invertebrates in particular: (1) studies that use end points across multiple levels of biological organization, including an ecosystem level approach where appropriate, (2) multiple species studies that produce comparable data across phylogenetic groups, and (3) determination of the modifying (i.e. antagonistic, additive or synergistic) effects of biotic and abiotic factors on the impact of ionizing radiation. It is essential that all of these issues are examined in the context of well-defined radiation exposure and total doses received and consider the life stages and life span of the species studied. The review also provides future directions for studies in this stimulating area of research to protect human and environmental health.     

Radiodermatitis as a consequence of radiation recall induced by acyclovir: case report

BackgroundRadiation recall dermatitis (RRD) is an inflammatory reaction in an area of the skin previously irradiated for cancer treatment. The reaction usually occurs following the administration of a cytotoxic drug. Manifestations range from mild to severe, resulting in tissue necrosis. It is treated with removal of the probable causative agent, daily dressings and surgical debridement of the necrotic area.Case presentationA 54-year-old woman had a previous diagnosis of intraductal carcinoma in situ, and had been submitted to lumpectomy and adjuvant radiotherapy and hormonal therapy. One year after surgery, sores suggestive of herpes zoster infection developed, and treatment with acyclovir was started. At the same time, there was the onset of pain and fever. In the skin area previously irradiated, there was breast hardening, skin infiltration and serosanguinolent discharge. An incisional biopsy was performed to rule out radioinduced sarcoma. The patient was treated with surgical debridement.ConclusionsThis case report describes acyclovir as a possible trigger of RRD, a rare condition that could have been mistaken for an eruption with other causes. In this case, the dermatitis reaction was confined to the previously irradiated area of the skin, which suggested radiation recall. A better understanding of the condition’s mechanism and about the possible joint effects of drugs and radiotherapy on the skin is necessary.     

Exploring the link between ceramide and ionizing radiation

The aim of radiotherapy is to eradicate cancer cells with ionizing radiation; tumor cell death following irradiation can be induced by several signaling pathways, most of which are triggered as a consequence of DNA damage, the primary and major relevant cell response to radiation. Several lines of evidence demonstrated that ceramide, a crucial sensor and/or effector of different signalling pathways promoting cell cycle arrest, death and differentiation, is directly involved in the molecular mechanisms underlying cellular response to irradiation. Most of the studies strongly support a direct relationship between ceramide accumulation and radiation-induced cell death, mainly apoptosis; for this reason, defining the contribution of the multiple metabolic pathways leading to ceramide formation and the causes of its dysregulated metabolism represent the main goal in order to elucidate the ceramide-mediated signaling in radiotherapy. In this review, we summarize the current knowledge concerning the different routes leading to ceramide accumulation in radiation-induced cell response with particular regard to the role of the enzymes involved in both ceramide neogenesis and catabolism. Emphasis is placed on sphingolipid breakdown as mechanism of ceramide generation activated following cell irradiation; the functional relevance of this pathway, and the role of glycosphingolipid glycohydrolases as direct targets of ionizing radiation are also discussed. These new findings add a further attractive point of investigation to better define the complex interplay between sphingolipid metabolism and radiation therapy.     

Health risks of low dose ionizing radiation in humans: a review

Radiobiologists have been struggling to estimate the health risks from low doses of radiation in humans for decades. Health risks involve not only neoplastic diseases but also somatic mutations that may contribute to other illnesses (including birth defects and ocular maladies) and heritable mutations that may increase the risk of diseases in future generations. Low dose radiation-induced cancer in humans depends on several variables, and most of these variables are not possible to correct for in any epidemiologic study. Some of the confounding factors include (i) interaction of radiation with other physical (UV light), chemical, and biological mutagens and carcinogens in a synergistic manner; (ii) variation in repair mechanisms that depend on dose; (iii) variation in sensitivity of bystander cells to subsequent radiation exposure that depends on whether they have been pre- or postirradiated; and (iv) variation in adaptive response that depends on radiation doses and protective substances (antioxidants). In our opinion, both the linear no-threshold-response and the threshold-response models might not be suitable in predicting cancer risk at low radiation doses in a quantitative sense. Low doses of ionizing radiation should not be considered insignificant for risks of somatic and heritable mutations and neoplastic and nonneoplastic diseases in humans.     

Evaluation of a ventricular septal defect in an orangutan: a case report

A 15-year-old male Sumatran orangutan (Pongo pymaeus abeli) with a history of an interventricular septal defect was evaluated with cardiac catheterization and two-dimensional echocardiography. Results demonstrated that by Homo sapiens standards the right heart pressures were normal. The oxygen saturations were consistent with a small ventricular septal defect. Echocardiography demonstrated a slight enlargement of the right ventricle.     

Membrane effects of ionizing radiation and hyperthermia

Results of numerous studies demonstrate that membranes are important sites of cell damage by both ionizing radiation and hyperthermia. Modification of membrane properties (mainly lipid fluidity) affects the cellular responses to radiation and hyperthermia but former concepts that membrane rigidification sensitizes cells to radiation while membrane fluidization potentiates hyperthermic damage have now been seriously challenged. It seems that the effects of membrane fluidity on cell responses to hyperthermia and radiation are due to an indirect influence on functional membrane proteins. The major role of lipid peroxidation in radiation damage to membranes has also been questioned. The existing evidence makes it unlikely that the interaction between radiation and hyperthermia is determined by the action of both agents on the same membrane components.     

ELF non ionizing radiation changes the distribution of the inner chemical functional groups in human epithelial cell (HaCaT) culture

Human skin cell culture (HaCaT) that has been exposed to an AC magnetic field undergoes detectable changes in its biochemical properties and shapes. Such changes were observed by infrared wavelength-selective scanning near-field optical microscopy with a resolution of 80-100 nm. We specifically investigated the changes in the distribution of the inner chemical functional groups and in the cell morphology induced by a 24 h exposure to a 1 mT (rms), 50 Hz sinusoidal magnetic field in a temperature regulated solenoid. These results further accentuate the crucial questions, raised by several recent studies, about the impact of low-frequency electromagnetic field on human cells.     

密切接触宠物兔后幼儿鼻孔周围体癣1例

报道1例密切接触宠物兔后发生在幼儿双侧鼻孔周围及上唇部的体癣。患儿4岁,因“鼻唇部红斑、鳞屑、伴瘙痒10余日”就诊。取皮屑镜检见真菌菌丝及毳毛内孢子,培养见棒形分隔大分生孢子、葡萄串状小分生孢子及螺旋菌丝。尿素酶试验阳性、毛发穿孔试验阳性,鉴定为须癣毛癣菌。经内服伊曲康唑胶囊和外用萘替芬酮康唑乳膏治疗6d后红斑瘙痒明显减轻,34d后皮损消退。复查真菌阴性。     

Down syndrome and ionizing radiation: causal effect or coincidence

Annual and monthly prevalence of Down's Syndrome has been analyzed in Belarus for a 19-year period (1981 to 1999). The distribution of 2786 DS cases during this period showed no significant long-term prevalence trend. Meanwhile, 2 marked increases of DS prevalence were registered in 1987 and 1990. The most remarkable annual increases were observed in 1987 in Minsk city, in Vitebsk oblast (considered as contamination-free administrative district) and in Minsk oblast (partially contaminated area), data not shown in the text. Much more marked and significant increases were recorded in January 1987, in Minsk city, Gomel oblast and Minsk oblast. However it is impossible to establish a causal relationship between these clusters of DS and exposure to the Chernobyl fallout, at a geographical level. The presence of such a cluster 9 months after the explosion in one of the most exposed area (Gomel oblast) should incite to careful conclusions and prompt further studies.     

Genomic damage in children accidentally exposed to ionizing radiation: a review of the literature

During the last decade, our knowledge of the mechanisms by which children respond to exposures to physical and chemical agents present in the environment, has significantly increased. Results of recent projects and programmes focused on children's health underline a specific vulnerability of children to environmental genotoxicants. Environmental research on children predominantly investigates the health effects of air pollution while effects from radiation exposure deserve more attention. The main sources of knowledge on genome damage of children exposed to radiation are studies performed after the Chernobyl nuclear plant accident in 1986. The present review presents and discusses data collected from papers analyzing genome damage in children environmentally exposed to ionizing radiation. Overall, the evidence from the studies conducted following the Chernobyl accident, nuclear tests, environmental radiation pollution and indoor accidental contamination reveals consistently increased chromosome aberration and micronuclei frequency in exposed than in referent children. Future research in this area should be focused on studies providing information on: (a) effects on children caused by low doses of radiation; (b) effects on children from combined exposure to low doses of radiation and chemical agents from food, water and air; and (c) specific effects from exposure during early childhood (radioisotopes from water, radon in homes). Special consideration should also be given to a possible impact of a radiochemical environment to the development of an adaptive response for genomic damage. Interactive databases should be developed to provide integration of cytogenetic data, childhood cancer registry data and information on environmental contamination. The overall aim is to introduce timely and efficient preventive measures, by means of a better knowledge of the early and delayed health effects in children resulting from radiation exposure.     

Low doses of ionizing radiation and circulatory diseases: a systematic review of the published epidemiological evidence

Recent analyses of mortality among atomic bomb survivors have suggested a linear dose-response relationship between ionizing radiation and diseases of the circulatory system for exposures in the range 0-4 Sv. If confirmed, this has substantial implications. We have therefore reviewed the published literature to see if other epidemiological data support this finding. Other studies allowing a comparison of the rates of circulatory disease in individuals drawn from the same population but exposed to ionizing radiation at different levels within the range 0-5 Gy or 0-5 Sv were identified through systematic literature searches. Twenty-six studies were identified. In some, disease rates among those exposed at different levels may have differed for reasons unrelated to radiation exposure, while many had low power to detect effects of the relevant magnitude. Among the remainder, one study found appreciable evidence that exposure to low-dose radiation was associated with circulatory diseases, but five others, all with appreciable power, did not. We conclude that the other epidemiological data do not at present provide clear evidence of a risk of circulatory diseases at doses of ionizing radiation in the range 0-4 Sv, as suggested by the atomic bomb survivors. Further evidence is needed to characterize the possible risk.