Objective:To investigate the radiation-induced abscopal effect in terms of oxidative stress, apoptosis and DNA damage in the spleen cells following cranial X-rays irradiation of rats.Methods:Rats were cranially irradiated using 2 Gy X-rays. Another group was whole-body irradiated with 2 Gy X-rays and a third group was exposed to scattered radiation (measured to be 3 mGy). 24 hours following irradiation, sections from the spleen of the rats were dissected as well as plasma samples. The samples were examined for the desired endpoints.Results:The cranially irradiated animals showed a significant increase in the levels of glutathione, superoxide dismutase and catalase with no significant change in the lipid peroxidation product in the spleen cells with a significant increase in the C-reactive protein level the plasma. Apoptotic cell death in the spleen cells was demonstrated as indicated by the decrease of Bcl-2; the increase of p53, Bax, caspase-3 and caspase-8 and induction of DNA damage in the spleen in bo...

An important stage in tumorigenesis is the ability of precancerous cells to escape natural anticancer signals. Apoptosis can be selectively induced in transformed cells by neighboring normal cells through cytokine and ROS/RNS signaling. The intercellular induction of apoptosis in transformed cells has previously been found to be enhanced after exposure of the normal cells to very low doses of both low- and high-LET ionizing radiation. Low-LET ultrasoft X rays with a range of irradiation masks were used to vary both the dose to the cells and the percentage of normal cells irradiated. The results obtained were compared with those after α-particle irradiation. The intercellular induction of apoptosis in nonirradiated src-transformed 208Fsrc3 cells observed after exposure of normal 208F cells to ultrasoft X rays was similar to that observed for γ rays. Intercellular induction of apoptosis was stimulated by irradiation of greater than 1% of the nontransformed 208F cells and increased with the fraction of cells irradiated. A maximal response was observed when ∼10–12% of the cells were irradiated, which gave a similar response to 100% irradiated cells. Between 1% and 10%, high-LET α particles were more effective than low-LET ultrasoft X rays in stimulating intercellular induction of apoptosis for a given fraction of cells irradiated. Scavenger experiments show that the increase in intercellular induction of apoptosis results from NO• and peroxidase signaling mediated by TGF-β. In the absence of radiation, intercellular induction of apoptosis was also stimulated by TGF-β treatment of the nontransformed 208F cells prior to coculture; however, no additional increase in intercellular induction of apoptosis was observed if these cells were also irradiated. These data suggest that the TGF-β-mediated ROS/RNS production reaches a maximum at low doses or fluences of particles, leading to a plateau in radiation-stimulated intercellular induction of apoptosis at higher doses.

The main goal of this work is to fabricate a biocomposite material of hydroxyapatite (HA) and polylactic acid (PLA) loaded with different concentrations of curcumin for using in bone tissue scaffold engineering. PLA-HA-curcumin biocomposite was prepared via the precipitation method with PLA/HA ratio of 80/20 wt% and different ratios of curcumin. The structure and surface morphology of the prepared biocomposite were studied using Fourier Transform Infrared spectroscopy (FTIR), x-ray diffraction spectroscopy (XRD), transmission electron microscope (TEM) and scanning electron microscope (SEM). The bioactivity enhancement of the prepared HA-PLA biocomposite was examined after immersion in simulated body fluid (SBF) before and after addition of curcumin. Drug release of the HA-PLA biocomposite prepared with different concentrations of curcumin was studied in phosphate buffer solution. Our data confirm the nanostructure of the prepared HA-PLA biocomposite and show good miscibility and diffusion of curcumin inside the scaffold matrix. Furthermore, curcumin supplementation effectively enhanced the bioactivity of the HA-PLA biocomposite.

Purpose: To investigate the effect of whole body low-dose radiation (10 cGy of 6 MeV x-rays) given prior to a challenging dose of 2 Gy x-rays on adaptive response in the liver of rats Materials and Methods: Rats were either irradiated with 10cGy, 2Gy or 10cGy 24h prior to 2Gy (10cGy-2Gy irradiated). Liver samples were analysed for apoptosis,caspase-3, Bcl-2, by flow cytometery. DNA damage was determined by alkaline comet assay. The protein damage, lipid damage, and expression of endogenous antioxidants, Il-1β, Il-6, and TNF-α were determined by ELISA. Results: An increase in apoptosis paralleled with increase in DNA damage and expression of Il-1β, Il-6, and TNF-α, protein oxidation and lipid peroxidation were detected in all irradiated groups. The irradiated rats with 10cGy-2Gy and the 2Gy-irradiated showed the highest effect. The increase in oxidative damage of protein and lipid was accompanied with depletion of endogenous antioxidants. In all cases, the10cGy-2Gy irradiated group showed similar or higher effect than the 2Gy-irradiated group. Conclusions: Under the present experimental conditions, There is no evidence that 10cGy-irradiation protected the liver cells against a subsequent higher dose. The significant effect of 10 cGy-irradiation emphasizes the low-dose radiation associated risk.