Zirconium / Hafnium / Thorium / Rutherfordium / Fluoride complexation / Anion and cation exchange chromatography Summary. The fluoride complexation of the group-4 elements Zr, Hf and Rf, and of the pseudo-homolog Th, has been investigated in mixed HNO 3 /HF solutions by studying K d values on both cation exchange resins (CIX) and anion exchange resins (AIX) using the automated rapid chemistry apparatus ARCA. On the CIX, the four elements are strongly retained as cations below 10 Ϫ3 M HF. For Zr and Hf, the decrease of the K d values due to the formation of fluoride complexes occurs between 10 Ϫ3 M HF and 10 Ϫ2 M HF. For Rf and Th, this decrease is observed at one order of magnitude higher HF concentrations. On the AIX, for Zr and Hf, a rise of the K d values due to the formation of anionic fluoride complexes is observed between 10 Ϫ3 M HF and 10 Ϫ2 M HF, i.e. in the same range of HF concentrations where the decrease of the K d values on the CIX is observed, yielding a consistent picture. For Rf and Th, on the AIX, no rise of the K d values is observed even if the HF concentration is increased up to 1 M. By varying the concentration of the counter ion NO 3 Ϫ which is competing for the binding sites on the AIX resin, it could be shown, nevertheless, that Rf does form anionic fluoride complexes. Apparently, there is a more specific competition of NO 3 Ϫ with respect to [RfF x ] (xϪ4)Ϫ than with [ZrF y ] (yϪ4)Ϫ and [HfF z ] (zϪ4)Ϫ .

Most accelerator-based space radiation experiments have been performed with single ion beams at fixed energies. However, the space radiation environment consists of a wide variety of ion species with a continuous range of energies. Due to recent developments in beam switching technology implemented at the NASA Space Radiation Laboratory (NSRL) at Brookhaven National Laboratory (BNL), it is now possible to rapidly switch ion species and energies, allowing for the possibility to more realistically simulate the actual radiation environment found in space. The present paper discusses a variety of issues related to implementation of galactic cosmic ray (GCR) simulation at NSRL, especially for experiments in radiobiology. Advantages and disadvantages of different approaches to developing a GCR simulator are presented. In addition, issues common to both GCR simulation and single beam experiments are compared to issues unique to GCR simulation studies. A set of conclusions is presented as well as a discussion of the technical implementation of GCR simulation.

During space travel astronauts are exposed to a variety of radiations, including galactic cosmic rays composed of high-energy protons and high-energy charged (HZE) nuclei, and solar particle events containing low- to medium-energy protons. Risks from these exposures include carcinogenesis, central nervous system damage and degenerative tissue effects. Currently, career radiation limits are based on estimates of fatal cancer risks calculated using a model that incorporates human epidemiological data from exposed populations, estimates of relative biological effectiveness and dose-response data from relevant mammalian experimental models. A major goal of space radiation risk assessment is to link mechanistic data from biological studies at NASA Space Radiation Laboratory and other particle accelerators with risk models. Early phenotypes of HZE exposure, such as the induction of reactive oxygen species, DNA damage signaling and inflammation, are sensitive to HZE damage complexity. This review summarizes our current understanding of critical areas within the DNA damage and oxidative stress arena and provides insight into their mechanistic interdependence and their usefulness in accurately modeling cancer and other risks in astronauts exposed to space radiation. Our ultimate goals are to examine potential links and crosstalk between early response modules activated by charged particle exposure, to identify critical areas that require further research and to use these data to reduced uncertainties in modeling cancer risk for astronauts. A clearer understanding of the links between early mechanistic aspects of high-LET response and later surrogate cancer end points could reveal key nodes that can be therapeutically targeted to mitigate the health effects from charged particle exposures.

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Zafar F., Seidler S.B., Kronenberg A., Schild D. and Wiese C. Homologous recombination contributes to the repair of DNA double-strand breaks induced by high-energy iron ions. Radiat. Res.To test the contribution of homologous recombinational repair (HRR) in repairing DNA damaged sites induced by high-energy iron ions, we used: 1) HRR-deficient rodent cells carrying a deletion in the RAD51D gene and 2) syngeneic human cells impaired for HRR by RAD51D or RAD51 knockdown using RNA interference. We show that in response to iron ions, HRR contributes to cell survival in rodent cells, and that HRR-deficiency abrogates RAD51 foci formation. Complementation of the HRR defect by human RAD51D rescues both enhanced cytotoxicity and RAD51 foci formation. For human cells irradiated with iron ions, cell survival is decreased, and, in p53 mutant cells, the levels of mutagenesis are increased when HRR is impaired. Human cells synchronized in S phase exhibit more pronounced resistance to iron ions as compared with cells in G1 phase, and this increase in radioresistance is diminished by RAD51 knockdown. These results implicate a role for RAD51-mediated DNA repair (i.e. HRR) in removing a fraction of clustered lesions induced by charged particle irradiation. Our results are the first to directly show the requirement for an intact HRR pathway in human cells in ensuring DNA repair and cell survival in response to high-energy high LET radiation.3