Parental exposure of mice to radiation and chemicals causes a variety of adverse effects in the progeny, and the tumor-susceptibility phenotype is transmissible beyond the first postradiation generation. The induced rates of tumors were 100-fold higher than those known for mouse specific locus mutations. There were clear strain differences in the types of naturally-occurring and induced tumors and most of the latter were malignant. Another important finding was that germ-line exposure elicited very weak tumorigenic responses, but caused persistent hypersensitivity in the offspring for the subsequent development of cancer by the postnatal environment. Various disorders were induced in the offspring of mice exposed to radiation. Microsatellite mutations increase dose-dependently and accumulated for 58 generations in the offspring of male parental mice exposed to single dose of X-rays. Changes in gene expression also transmitted to further generations. Radiation-induced genomic instability in germ cells may enhance cancer and other disorders in next generation. In humans, a higher risk of leukemia and birth defects has been reported in the children of fathers who had been exposed to radionuclides in the nuclear reprocessing plants and to diagnostic radiation. These findings have not been supported in the children of atomic bomb survivors in Hiroshima and Nagasaki, who were exposed to higher doses of atomic radiation. However, long-term monitoring of children by Russian Federation Children's Center of Antiradiation Protection after Chernobyl accident shows higher prevalence of malignant neoplasm, mostly childhood cancer, malformation, and other disorders in the children of residents exposed to contaminated radionuclides (>556 kBq/m²). Persistent accumulation of genomic instability may cause various disorders in a further generation in human. This view will gain support from our mouse experiments, because the induced rate of solid tumors in the offspring of mice exposed to radiation is much higher than that of leukemia.

Adverse radiation effect (ARE) in the brain is the reactive inflammation, vasculitis, and necrosis that occurs as a complication of radiotherapy. There are two main categories of ARE that result in vasogenic cerebral edema: first, a residual irritant mass of the targeted lesion; and second, radiation-damaged perilesional normal brain tissue in a reactive state. Radiation injury leads to fibrinoid and coagulative necrosis of different cell types and fibrinoid necrosis and hyalinization of vessels. The clinical consequence of ARE is neurologic impairment secondary to vasogenic edema in the normal brain. Neuroimaging may aid in differentiating tumor recurrence from ARE. However, imaging studies are not definitive, and their utility in this setting remains controversial. The management of patients with ARE is dictated by symptom occurrence. The definitive management of symptomatic ARE is craniotomy and resection. Alternative therapies include bevacizumab, laser-interstitial thermal therapy, and reirradiation.

Introduction: Curcumin is a known antioxidant, preventing radiation damage including carcinogenesis. However, concentration and feeding schedule of curcumin in modification of radiation induced thymic lymphoma incidence in vivo model has not been studied. Materials and Methods: We report here modification of incidence of γ-radiation-induced thymic lymphoma in mice fed with different doses of curcumin (0.05 to 1*) in diet. Results: Female Swiss mice (6-8 weeks) fed with normal diet and exposed to 3 Gy whole body⁶⁰Co γ-irradiation (WBI) showed 85 * incidence of thymic lymphoma (TL) at 120 days post-irradiation. A concentration of 1 * curcumin was found the most effective in TL incidence prevention than other fed concentrations. The TL incidence was remarkably reduced when curcumin was fed to the mice before than after the radiation exposure. The incidence of TL was reduced to 63* in mice fed with 1* curcumin in diet for 3 weeks after exposure to WBI. On the other hand, when animals were fed with same concentration of curcumin for 2 weeks and 3 weeks before WBI, the TL incidence was reduced to 55* and 35*, respectively. Curcumin feeding resulted in significant prevention in micronucleus formation in the bone marrow, which was corroborated with inhibition in DNA damage quantified by comet assay. Moreover, significant prevention in DNA damage was also observed in the peripheral blood cells in curcumin fed and irradiated mice, which however, was not prominent in thymus. Curcumin was able to prevent apoptotic death in thymus and bone marrow 4 h after irradiation, which however, got attenuated at longer post-irradiation period (24 h). Conclusion: These results suggest modification of TL incidence by curcumin in irradiated mice involving DNA damage and apoptotic death mechanisms.

Introduction: Radiation exposure to brain is known to cause cognitive deficits. Aim of the current study was to investigate whether lithium protects against radiation. It was further investigated whether this protective effect is associated with neuritogenesis and altered Neural Cell Adhesion Molecule (NCAM) expression. Materials and Methods: Human neuroblastoma cell line, SK-N-MC was exposed to gamma radiation alone and after 24 h pretreatment with lithium. Cells were scored for viability by MTT assay and checked for apoptotic changes by flow cytometry (FCM). Geimsa stained cells were scored for number of cells bearing neuritis and length of neuritis. Real time PCR was used to measure levels of NCAM transcript in the cells. Results: Radiation exposure of 5 Gray resulted in significant decrease in cell viability. Pretreatment with lithium rescued cells from radiation- induced toxicity as indicated by MTT assay and by FCM analysis. Morphological observations suggested radiation caused increase in neurite lengths and decrease in number of cells bearing neurites. This was reversed by lithium treatment. Several fold decrease in NCAM expression was observed post radiation exposure which was reversed by lithium pretreated cells. Conclusion: Lithium protects neuronal cells against radiation damage. The protective effect of lithium is associated with change in differentiation status of cells as indicated by neuritogenesis and with alteration in expression of NCAM, a molecule known to be associated with neurite formation.

This paper reports the development of an X-ray imaging facility on Indus-2, synchrotron source at RRCAT, India and its potential applications in biomedical imaging. Indus-2 is country's first third-generation synchrotron source operating at energy of 2.5 Gev and current ~ 200 mA. It is a source of wide spectrum photon beam with very high flux and brilliance; therefore, it can be used for a variety of research such as spectroscopy, diffraction, imaging, lithography, and radiation processing. The development of X-ray imaging beamline here and implementation of several advanced imaging techniques, such as phase-contrast radiography, laminography, tomography, real-time imaging, and fluorescence imaging, has opened up new opportunities for characterization and study of soft tissue and biomaterials. This state of the art national facility is open to users for research in materials, biomedical and microtomography applications.