Measurement of 16O5+ Induced L X-Ray Production Cross Sections for Gold

The characteristic Ll, Lα, Lβ and Lγx-rays of Au and energy shifts produced by 20–50MeV 16O5+ beams on a thick Au ilm are measured with a Si (Li) detector. Cross-section ratios of σ(Ll)/σ(Lα), σ(Lβ)/σ(Lα) andσ(Lγ)/σ(Lα) versus O5+ energy show that consistent calculations yield considerably better agreements. Energy shifts Ll, Lα, Lβ and Lγ x-rays of Au target increase with more incidence energy. The main application for these measurements is multi-element trace analysis through particle induced x-ray emission.

Measurement of the inelastic branch of the O-14(alpha, p)F-17 reaction: Implications for explosive burning in novae and x-ray bursters

A measurement of the inelastic component of the key astrophysical resonance in the 14O(α,p)17F reaction for burning and breakout from hot carbon-nitrogen-oxygen (CNO) cycles is reported. The inelastic component is found to be comparable to the ground-state branch and will enhance the 14O(α,p)17F reaction rate. The current results for the reaction rate confirm that the 14O(α,p)17F reaction is unlikely to contribute substantially to burning and breakout from the CNO cycles under novae conditions. The reaction can, however, contribute strongly to the breakout from the hot CNO cycles under the more extreme conditions found in x-ray bursters.

Electron transfer in fast atomic collisions in the presence of an x-ray laser

We consider electron capture in fast collisions between a proton and hydrogen in the presence of an intense x-ray laser whose angular frequency omega is close to v(2)/2, where v is the collision velocity. We show that in such a case laser-induced capture becomes possible and that the latter proceeds via both induced photon emission and photon absorption channels and can, in principle, compete with kinematic and radiative electron capture.

NADPH oxidase-mediated generation of reactive oxygen species: A new mechanism for X-ray-induced HeLa cell death

Oxidative damage is an important mechanism in X-ray-induced cell death. Radiolysis of water molecules is a source of reactive oxygen species (ROS) that contribute to X-ray-induced cell death. In this study, we showed by ROS detection and a cell survival assay that NADPH oxidase has a very important role in X-ray-induced cell death. Under X-ray irradiation, the upregulation of the expression of NADPH oxidase membrane Subunit gp91(phox) was dose-dependent. Meanwhile, the cytoplasmic subunit p47(phox) was translocated to the cell membrane and localized with p22(phox) and gp91(phox) to form reactive NADPH oxidase. Our data Suggest, for the first time, that NADPH oxidase-mediated generation of ROS is an important contributor to X-ray-induced cell death. This suggests a new target for combined gene transfer and radiotherapy.

L-shell x-ray yields and production cross sections of Zr and Mo bombarded by slow highly charged Ar16+ ions

The L-shell x-ray yields of Zr and Mo bombarded by slow Ar16+ ions are measured. The energy of the Ar16+ ions ranges from about 150keV to 350keV. The L-shell x-ray production cross sections of Zr and Mo are extracted from these yields data. The explanation of these experimental results is in the framework of the adiabatic directionization and the binding energy modified BEA approximation. We consider, in the slow asymmetric collisions such as Ar and Mo/Zr, the transient united atoms (UA) are formed during the ion-surface interaction and the direct-ionization is the main mechanism for the inner-shell vacancy production. Generally, the theoretical results are in good agreement with the experimental data.

Antioxidant N-acetylcysteine attenuates the acute liver injury caused by X-ray in mice

The aim of this study was to evaluate the protective effects of different doses and administration modes of N-acetylcysteine (NAC) against X-ray-induced liver damage in mice. Kun-Ming mice were divided into four groups, each composed of six animals: two control groups and two NAC-treated groups. An acute study was carried out to determine alterations in lipid peroxidation (determined by measuring malondiadehyde (MDA) level), glutathione (GSH) content and superoxide dismutase (SOD) activity (assayed by colorimetric method), and DNA damage (characterized by DNA-single strand break using with comet assay) as well as cell apoptosis (measured by flow cytometry) at 12 h after irradiation. The results showed that there were dose-related decreases in MDA level, DNA damage and cell apoptosis, and dose-dependent increases in GSH content and SOD activity in all NAC-treated groups compared to control groups, indicating that pre-treatment or post-treatment with NAC significantly attenuates the acute liver damage caused by X-ray. In addition, significant positive correlations were observed between MDA level and DNA damage or cell apoptosis, implying that lipid peroxidation plays a major role in X-ray-induced liver injury. The data suggest that NAC exerts its radioprotective effect by counteracting accumulated reactive oxygen species in the liver through its properties as a direct antioxidant and a GSH precursor, when administered before or after X-ray irradiation.

Study on the apoptosis and Bcl-2/Bax expression of human hepatoma SMMC-7721 cells after exposure to heavy-ion and X-ray irradiations

This study is aimed at observing the apoptosis and Bcl-2/Bax gene expression of mammalian cells following heavy-ion and X-ray irradiations. Exponentially growing human hepatoma SMMC-7721 cells cultured in vitro were irradiated with a C-12 ion beam of 50 MeV/u (corresponding to a LET value of 44.56 keV/mu m) from Heavy Ion Research Facility in Lanzhou (HIRFL) at doses varying from 0 to 3 Gy. The X-ray irradiation (8 MV) was performed in the therapy unit of the General Hospital of the Lanzhou Military Area. Survival fractions of irradiated cells at various doses were measured by means of MTT assay. Apoptotic cells after irradiation were analyzed with fluorescence microscope and flow cytometer (FCM). Immuno-histological assay were applied to detect the expression of Bcl-2/Bax genes in the irradiated cells. The survival fraction of SMMC-7721 cells decreased gradually (vs. control p<0.05) with increasing the dose of the carbon ion beam more obviously than X-ray irradiation, and the carbon ion irradiation efficiently induced cell apoptosis and significantly promoted the expression of Bax gene while Bcl-2 gene expression was restrained. High-LET heavy ion beam would induce cell apoptosis effectively than low-LET X-ray, and the apoptosis rate is correlated with the transcription of Bcl-2/Bax and the ratio of Bcl-2/Bax in human hepatoma SMMC-7721 cells after irradiation to heavy ion beam.

X-ray spectroscopy of hollow argon atoms formed on a beryllium surface

The X-rays induced during interaction of highly charged argon ions with a beryllium surface are reported. It is found that the K shell X-ray yield of single particle during interaction of hydrogen-like argon ions was 3.6 x 10(-3), which is five orders more than that of heliumlike argon ions. Moreover, due to the screening the 2s electron, no K X-ray was emitted during interaction of lithium-like argon ions with the beryllium surface. It is also found that the X-ray spectrum induced by Ar17+ interacting with residual gases is very different from that induced by Ar17+ interacting with the surfaces, that provided an experimental evidence for the existence of the hollow atoms below the surface.

Potentiality of phosphorylation of BRCA1 at Ser 1524 to activate p21 in response to X-ray irradiation

The breast and ovarian cancer susceptibility gene BRCA1 encodes a nuclear phosphoprotein, which functions as a tumor suppressor gene. Many studies suggested that multiple functions of BRCA1 may contribute to its tumor suppressor activity, including roles in cell cycle checkpoints, apoptosis and transcription. It is postulated that phosphorylation of BRCA1 is an important means by which its cellular functions are regulated. In this study, we employed phospho-Ser-specific antibody recognizing Ser-1524 to study BRCA1 phosphorylation under conditions of DNA damage and the effects of phosphorylation on BRCA1 functions. The results showed that 10 Gy X-ray treatment significantly induced phosphorylation of Ser-1524 but not total BRCA1 protein levels. The expression both of p53 and p21 increased after irradiation, but ionizing radiation (IR) -induced activation of p21 was prior to that of p53. The percentages of G0/G1 phase remarkably increased after IR. In addition, no detectable levels of 89 kDa fragment of PARP, a marker of apoptotic cells, were observed. Data implied that IR-induced phosphorylation of BRCA1 at Ser-1524 might activatep21 protein, by which BRCA1 regulated cell cycle, but play no role in apoptosis.