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[Molecular and cellular mechanisms of late radiation injuries].

Late radiation damages arise more often in nonproliferating or slow proliferating tissues after local irradiation in large (intolerable) doses of ionizing radiation. Obviously the late radiation effects are induced by radiation damages to capillaries and disturbances of microcirculation in tissues. This is a basis for tissue hypoxia, "oxidative stress" and loss of parenchyma cells. The direct radiation effect on parenchyma cells has as a rule little importance for production of late radiation damages. Other type of late radiation damages can be discovered after sublethal irradiation of whole body. This is a cause of decrease of life span. In this case the important factors are also damages of vessels, disturbances in microcirculation and loss of parenchyma cells in "target" organs especially in neuroendocrine and immune systems. The new data on the possibility to decrease the late radiation damages after local or whole body irradiation using postradiation treatment with pulsed electric field (PEF) are considered. Mechanisms of PEF effects are explained in terms of its ability to induce nitric oxide production which causes intensification of blood microcirculation, as well as increase in SOD production and activity of repair enzymes.

Animals↗
PubMed2004

Uptake of 18F-fluorocholine, 18F-fluoroethyl-L-tyrosine, and 18F-FDG in acute cerebral radiation injury in the rat: implications for separation of radiation necrosis from tumor recurrence.

UNLABELLED: Differentiation between posttherapy radiation necrosis and recurrent tumor in humans with brain tumor is still a difficult diagnostic task. The new PET tracers (18)F-fluoro-ethyl-l-tyrosine (FET) and (18)F-fluorocholine (N,N-dimethyl-N-(18)F-fluoromethyl-2-hydroxyethylammonium [FCH]) have shown promise for improving diagnostic accuracy. This study assessed uptake of these tracers in experimental radiation injury. METHODS: In a first model, circumscribed lesions were induced in the cortex of 35 rats using proton irradiation of 150 or 250 Gy. After radiation injury developed, uptake of (18)F-FET, (18)F-FCH, and (18)F-FDG was measured using autoradiography and correlated with histology and disruption of the blood-brain barrier as determined with Evans blue. In a second model, uptake of the tracers was assessed in acute cryolesions, which are characterized by the absence of inflammatory cells. RESULTS: Mean (18)F-FET, (18)F-FCH, and (18)F-FDG standardized uptake values in the most active part of the radiation lesion and the contralateral normal cortex (in parentheses) were 2.27 +/- 0.46 (1.42 +/- 0.23), 2.52 +/- 0.42 (0.61 +/- 0.12), and 6.21 +/- 1.19 (4.35 +/- 0.47). The degree of uptake of (18)F-FCH and (18)F-FDG correlated with the density of macrophages. In cryolesions, (18)F-FET uptake was similar to that in radiation lesions, and (18)F-FCH uptake was significantly reduced. CONCLUSION: Comparison of tracer accumulation in cryolesions and radiation injuries demonstrates that (18)F-FET uptake is most likely due to a disruption of the blood-brain barrier alone, whereas (18)F-FCH is additionally trapped by macrophages. Uptake of both tracers in the radiation injuries is generally lower than the published uptake in tumors, suggesting that (18)F-FET and (18)F-FCH are promising tracers for separating radiation necrosis from tumor recurrence. However, the comparability of our data with the literature is limited by factors such as different species and acquisition protocols and modalities. Thus, more studies are needed to settle this issue. Nevertheless, (18)F-FCH and (18)F-FET seem superior to (18)F-FDG for this purpose.

Acute Disease↗
PubMed2002

A systematic review of the literature reporting the application of hyperbaric oxygen prevention and treatment of delayed radiation injuries: an evidence based approach.

The treatment of delayed radiation injuries (soft tissue and bony radiation necrosis) is one of thirteen conditions approved by the Hyperbaric Oxygen Therapy Committee of the Undersea and Hyperbaric Medical Society as appropriate indications for hyperbaric oxygen (HBO2). This paper provides a systematic review of the literature reporting the results of HBO2 therapy in the treatment and/or prophylaxis of delayed radiation injury. Since the introduction of the concept of evidence based medicine, the medical community in general has set out to apply more critical and stringent standards in evaluating published support for therapeutic interventions. Evidence based medicine is designed to discover the best evidence available and apply it in daily practice for treatment of the individual patient. The preferred level of evidence is the randomized controlled trial, however, other evidence has merit as well. In this review, seventy-four publications are represented reporting results of applying HBO2 in the treatment or prevention of radiation injuries. These are appraised in an evidence-based fashion by applying three established systems of evaluation. All but seven of these publications report a positive result when HBO2 is delivered as treatment for or prevention of delayed radiation injury. These results are particularly impressive in the context of alternative interventions. Without HBO2, treatment often requires radical surgical intervention, which is likely to result in complications. Other alternatives including drug therapies are rarely reported, and for the most part have not been the subject of randomized controlled trials. Based on this review, HBO2 is recommended for delayed radiation injuries for soft tissue and bony injuries of most sites. Of note, an increasing body of evidence supports HBO2 for radiation-induced necrosis of the brain. For other radiation-induced neurological injuries, additional study is required before recommendations for routine hyperbaric therapy can be made.

Breast Diseases↗
PubMed2004

Post-irradiation approaches to treatment of radiation injuries in the context of radiological terrorism and radiation accidents: a review.

PURPOSE: Events of the recent past have focused attention on the possibility of radiological (nuclear) terrorism and on the implications of such terrorist threats for radiation accident preparedness. This review discusses recent advances in the knowledge about how radiation injuries from such events might be treated pharmacologically, and the practical barriers to clinical utilization of these approaches. CONCLUSIONS: A wide range of pharmacological approaches are being developed in the laboratory that could greatly expand the ability to treat acute and chronic radiation injuries. However, there are currently a variety of practical and legal barriers that would prevent the actual clinical use of most of the approaches. There are also the potential weaknesses in most of the current programmes for dealing with the consequences of radiation accidents or nuclear terrorism, including the absence of widespread radiation biodosimetry capabilities and the resulting inability to triage. If a major radiation accident or terrorist event occurs, the lack of biodosimetry and treatment capabilities will be compounded by widespread public fear of 'radiation'.

Abnormalities, Radiation-Induced↗
PubMed2002

Radiation injury of the lung after three-dimensional conformal radiation therapy.

OBJECTIVE: The objective of this study is to describe the CT patterns of radiation injury in the lungs of patients who have undergone three-dimensional (3D) conformal radiation therapy (CRT). MATERIALS AND METHODS: Over a 36-month period, the chest CT scans of 19 patients with non-small cell lung cancer who were treated with 3D CRT were reviewed. CT scans were evaluated for findings of radiation injury (ground-glass opacities, consolidation, bronchiectasis, and volume loss). The presence, extent, and distribution of these findings were reached by consensus. RESULTS: Radiation pneumonitis limited to a small area immediately around the tumor was present in all patients who were imaged within 3 months after completion of the treatment (n = 7). Radiation-induced fibrosis occurred in all patients (n = 19). Three distinct patterns of fibrosis were consistently present, and these were classified as modified conventional, masslike, and scarlike. Modified conventional fibrosis (consolidation, volume loss, and bronchiectasis similar to, but less extensive than, conventional radiation fibrosis) was seen in five patients. Masslike fibrosis (focal consolidation with traction bronchiectasis limited to the site of the original tumor) was seen in eight patients. Scarlike fibrosis (linear opacity in the region of the original tumor associated with moderate to severe volume loss) was seen in six patients. CONCLUSION: Three-dimensional conformal radiation therapy results in three patterns of radiation fibrosis that differ from the conventional radiation-induced lung injury. Knowledge of the full spectrum of these manifestations is useful in the correct interpretation of CT scans after 3D CRT.

Adult↗
PubMed1977

Roentgen manifestations of radiation injury to the gastrointestinal tract.

Radiation injury of the gastrointestinal tract requires a minimum dose of 4200 to 4500 rads. The symptoms and signs of radiation injury usually appear within 6 to 24 months following therapy. The radiation induced changes include mucosal atrophy and ulceration associated with an obliterative endarteritis in the supportive vasculo-connective tissue. The roentgen manifestations are those of an ischemic process but may also mimic those of recurrent malignant disease. Obstruction, hemorrhage, and fistula formation are common complications. Surgery is frequently required. The morbidity and mortality is considerable.

Colon↗
PubMed2002

Cytokine-based treatment of radiation injury: potential benefits after low-level radiation exposure.

The use of growth factors (GFs) in the treatment of radiation injury has focused on enhancing recovery from acute radiation syndrome. A number of new GFs have shown significant in vivo and in vitro preclinical efficacy; some of these have recently been approved by the Food and Drug Administration, some are in various phases of clinical trials, and some are moving through preclinical evaluations. The most promising new GFs in the context of enhancing the viability of irradiated hematopoietic stem cells (HSCs) are flt-3L, c-kitL, and c-mplL. These GFs, as well as interleukin 3 (IL-3), have been shown to maintain viability, suppress apoptosis, and promote the clonal growth of primitive murine and human hematopoietic progenitor cells. Further evidence suggests that these GFs may also act in synergy with each other. Additionally, three families of chimeric proteins that consist of dual GF receptor (R) agonists have been engineered: myelopoietin, promegapoietin, and progenipoietin. These proteins activate the IL-3 and granulocyte colony-stimulating factor Rs, the IL-3 and mpl Rs, and the flt-3L and granulocyte colony-stimulating factor Rs, respectively. The preclinical data indicate that the chimeric GFR agonists are potent stimulators of hematopoiesis in myelosuppressed nonhuman primates and can effectively alleviate acute radiation syndrome in animals. Acute or protracted low-level radiation exposure does not require the extensive clinical care necessary following radiation-induced myelosuppression. The main question is whether these new GFs will allow for enhanced repair of radiation-induced chromosome aberrations while promoting early survival of HSCs. Other questions include the following: Will an early, brief exposure to GFs suppress p53-dependent apoptosis and induce expression of bcl-2 with a concomitant enhancement of DNA repair capacity? What is the effect of GF stimulation of irradiated HSCs on p53 cell cycle checkpoint activity? Will GFs promote survival of "transformed" cells that would otherwise be eliminated by p53 activation of apoptosis-promoting genes? Relevant animal models and access to appropriate GFs will be required to answer these questions.

Animals↗
PubMed2006

Orazipone, a locally acting immunomodulator, ameliorates intestinal radiation injury: a preclinical study in a novel rat model.

PURPOSE: Intestinal radiation injury (radiation enteropathy) is relevant to cancer treatment, as well as to radiation accidents and radiation terrorism scenarios. This study assessed the protective efficacy of orazipone, a locally-acting small molecule immunomodulator. METHODS AND MATERIALS: Male rats were orchiectomized, a 4-cm segment of small bowel was sutured to the inside of the scrotum, a proximal anteperistaltic ileostomy was created for intraluminal drug administration, and intestinal continuity was re-established by end-to-side anastomosis. After three weeks postoperative recovery, the intestine in the "scrotal hernia" was exposed locally to single-dose or fractionated X-radiation. Orazipone (30 mg/kg/day) or vehicle was administered daily through the ileostomy, either during and after irradiation, or only after irradiation. Structural, cellular, and molecular aspects of intestinal radiation toxicity were assessed two weeks after irradiation. RESULTS: Orazipone significantly ameliorated histologic injury and transforming growth factor-beta immunoreactivity levels, both after single-dose and fractionated irradiation. Intestinal wall thickness was significantly reduced after single-dose and nonsignificantly after fractionated irradiation. Mucosal surface area and numbers of mast cells were partially restored by orazipone after single-dose irradiation. CONCLUSIONS: This work (1) demonstrates the utility of the ileostomy rat model for intraluminal administration of response modifiers in single-dose and fractionated radiation studies; (2) shows that mucosal immunomodulation during and/or after irradiation ameliorates intestinal toxicity; and (3) highlights important differences between single-dose and fractionated radiation regimens.

Animals↗
PubMed1992

Therapies for radiation injuries: research perspectives.

Exposure to radiation damages the immune, hematopoietic, and gastrointestinal components of the host defense system. This may lead to serious endogenous or exogenous infections. When radiation injury is combined with other physical trauma, e.g., burn or wound, the resulting damage to these systems is synergistic, and treatment for infection requires multiple approaches. This paper reviews successful single and combined therapeutic modalities for infections in irradiated mice and irradiated mice inflicted with trauma that are currently conducted at the Armed Forces Radiobiology Research Institute. The models of endogenous and exogenous infection and combined injury are described. The management of wounds infected with bacteria, exogenous systemic infection due to gram-negative enteric bacteria, and the chemoprophylaxis of enteric-derived systemic infection with quinolones is described. Infections can be treated successfully with proper antimicrobial therapy. In gamma- and neutron-irradiated mice, the immunomodulator trehalose dimycolate (TDM) was effective in treating endogenous infection. TDM with the antimicrobial ceftriaxone was effective in treating exogenous infection due to Klebsiella pneumoniae. Improvement in managing infection in irradiated and injured hosts will require further research using these diagnostic and therapeutic modalities. Accurate biological dosimetry is critical in determining if victims are at risk of developing infection. We found that radiation induced changes in plasma diamine oxidase activity; monitoring these changes was a useful indicator of the severity of radiation injury.

Adjuvants, Immunologic↗
PubMed1986

A T cell model for age-related loss of homeostasis: identification of the cell type responsible for age-related delay in recovery of the PHA-induced mitogenic response from radiation injury.

Immunologic recovery from radiation injury was used to assess age-related loss of immunologic homeostasis. Mice were exposed to 500 rad to determine whether macrophages, T helper cells and/or T responder cells were responsible for the age-related delay in recovery of PHA-induced mitogenesis. Recovery of macrophages was determined by facilitation of macrophage-deficient cultures, recovery of T helper cells by interleukin 2 production, and recovery of T responder cells by incorporation of tritiated thymidine. The results showed that in old mice macrophages are resistant to radiation and aging, T helper cells recover completely from radiation, and recovery is incomplete for T responder cells.

Aging↗
PubMed1998

[The modelling of local radiation injuries to the skin].

The models of local radiation injuries of skin--radiation ulcer, radiation epidermitis, radiation dermatitis in guinea-pigs and rabbits are developed. Experimental reproduction local radiation injuries by different doses, regimes and spices of ionizing irradiation was carried out. Detailed description of radiation action on skin is given. Pathomorphologic characteristic of radiation ulcers is given. Models may be used for pathogenesis learning and experimental therapy of local skin radiation injures.

Animals↗