Detrimental Effect Of Irradiation Research Articles

Molecular mechanisms of poor osseointegration in irradiated bone: In vivo study in a rat tibia model.

Radiotherapy is associated with cell depletion and loss of blood supply, which are linked to compromised bone healing. However, the molecular events underlying these effects at the tissue-implant interface have not been fully elucidated. This study aimed to determine the major molecular mediators associated with compromised osseointegration due to previous exposure to radiation. Titanium implants were placed in rat tibiae with or without pre-exposure to 20 Gy irradiation. Histomorphometric, biomechanical, quantitative polymerase chain reaction (qPCR) and enzyme-linked immunosorbent assay analyses were performed at 1 and 4 weeks after implantation. The detrimental effects of irradiation were characterized by reduced bone-implant contact and removal torque. Furthermore, pre-exposure to radiation induced different molecular dysfunctions such as (i) increased expression of pro-inflammatory (Tnf) and osteoclastic (Ctsk) genes and decreased expression of the bone formation (Alpl) gene in implant-adherent cells; (ii) increased expression of bone formation (Alpl and Bglap) genes in peri-implant bone; and (iii) increased expression of pro-inflammatory (Tnf) and pro-fibrotic (Tgfb1) genes in peri-implant soft tissue. The serum levels of pro-inflammatory, bone formation and bone resorption proteins were greater in the irradiated rats. Irradiation causes the dysregulation of multiple biological activities, among which perturbed inflammation seems to play a common role in hindering osseointegration.

Plastic Deformation in ODS Ferritic Alloys: A 3D Dislocation Dynamics Investigation

Abstract Discrete dislocation dynamics simulations were carried out to examine mechanical behavior of ferritic steel strengthened with Oxide Dispersion Strengthening (ODS) particles. Interplay of irradiation induced defect clusters and the ODS precipitates and its effect on the strain localization and hardening of the material is investigated. These simulations show that, in the absence of irradiation, the ODS particles act as an impediment to the dislocation motion and hence lead to greater strain localization, when subjected to uni-axial tensile deformation. After irradiation, however, it is seen that the presence of interstitial loops in the material reverses this trend. That is, presence of particles act against the detrimental effect of irradiation induced defect microstructure and helps in reducing strain localization. The hardening behavior also exhibits the same trend. Our study indicates that the irradiatio n induced hardening is suppressed by the presence of strengthening particles.

Oxidative stress and gamma radiation-induced cancellous bone loss with musculoskeletal disuse.

Exposure of astronauts in space to radiation during weightlessness may contribute to subsequent bone loss. Gamma irradiation of postpubertal mice rapidly increases the number of bone-resorbing osteoclasts and causes bone loss in cancellous tissue; similar changes occur in skeletal diseases associated with oxidative stress. Therefore, we hypothesized that increased oxidative stress mediates radiation-induced bone loss and that musculoskeletal disuse changes the sensitivity of cancellous tissue to radiation exposure. Musculoskeletal disuse by hindlimb unloading (1 or 2 wk) or total body gamma irradiation (1 or 2 Gy of (137)Cs) of 4-mo-old, male C57BL/6 mice each decreased cancellous bone volume fraction in the proximal tibiae and lumbar vertebrae. The extent of radiation-induced acute cancellous bone loss in tibiae and lumbar vertebrae was similar in normally loaded and hindlimb-unloaded mice. Similarly, osteoclast surface in the tibiae increased 46% as a result of irradiation, 47% as a result of hindlimb unloading, and 64% as a result of irradiation + hindlimb unloading compared with normally loaded mice. Irradiation, but not hindlimb unloading, reduced viability and increased apoptosis of marrow cells and caused oxidative damage to lipids within mineralized tissue. Irradiation also stimulated generation of reactive oxygen species in marrow cells. Furthermore, injection of alpha-lipoic acid, an antioxidant, mitigated the acute bone loss caused by irradiation. Together, these results showed that disuse and gamma irradiation, alone or in combination, caused a similar degree of acute cancellous bone loss and shared a common cellular mechanism of increased bone resorption. Furthermore, irradiation, but not disuse, may increase the number of osteoclasts and the extent of acute bone loss via increased reactive oxygen species production and ensuing oxidative damage, implying different molecular mechanisms. The finding that alpha-lipoic acid protected cancellous tissue from the detrimental effects of irradiation has potential relevance to astronauts and radiotherapy patients.

Iodine stress corrosion cracking of zircaloy: Laboratory data, a phenomenological model, and predictions of in-reactor behavior

Data from laboratory tests performed on unirradiated and irradiated Zircaloy have been used as the basis for developing a phenomenological model of iodine-induced stress corrosion crack initiation and growth. The model is capable of predicting the response of cladding subjected to complex loading conditions. Major features of the data incorporated into the model include the existence of a threshold stress, the effect of iodine concentration, temperature effects, the role of chemical inhomogeneities and mechanical flaws, crack initiation in smooth specimens, crack propagation rates as a function of stress intensity in flawed specimens, and the detrimental effect of irradiation. The major physical processes addressed by the model include intergranular stress corrosion cracking (SCC), transgranular SCC, ductile rupture, iodine penetration by surface diffusion along existing or incipient cracks, and stress and strain intensification and triaxiality caused by cracks or flaws. A probabilistic description of the size distribution of the flaws found in as-fabricated cladding is used as the basis for quantitatively extrapolating the laboratory test results to predict in-reactor cladding behavior. The in-reactor SCC resistance of a large fuel assembly is predicted to be substantially lower and more variable than that of small laboratory specimens.

The Influence of Immunization and Total Body X-Irradiation on Intracellular Digestion by Peritoneal Phagocytes

Summary Total body x-irradiation suppresses intracellular digestion of chicken erythrocytes by the peritoneal phagocytes of mice and rabbits. Such digestive function was normal on the second and eighteenth postirradiation days but was depressed on the sixth through the fourteenth day following 350-r total body irradiation of mice. When the irradiation dose was increased to 450 r, digestion of chicken erythrocytes by mouse phagocytes did not return to normal until the twenty-sixth day. The inhibition of phagocyte digestion of Candida guilliermondi followed the same pattern as observed with chicken red blood cells. Immunization with chicken erythrocytes caused an increase in the digestion of these cells by the phagocytes from mice and rabbits. The immunization-induced increase in digestive capacity was reversed by irradiation procedures that did not appreciably alter serum antibody titers. In vitro tests carried out in the presence of serum from immunized and immunized-irradiated rabbits revealed that the beneficial effect of immunization and the detrimental effect of irradiation on phagocyte digestion were due to alterations in the phagocytic cell and not due to the humoral changes that follow irradiation or immunization.