The main objective of the study was to characterise, by electron spin resonance (ESR) spectroscopy, novel halogen containing a* radicals. These species are formed by ?-irradiation in a variety of halogen containing systems at liquid nitrogen temperatures. In Chapter One, a brief description of the first halogen a* radical to be identified, the Vx centre in potassium chloride (C12.-), is given in order to illustrate the general magnetic properties of the species. The dependence of these properties on the host matrix is also described. Accepted radiation damage mechanisms are presented with particular reference to dihalogen a* radicals. Some theoretical aspects of the ESR experiment is discussed in Chapter Two which explains briefly some of the phenomena encountered in the study. Sample preparation and analysis are also mentioned. Chapter Three describes the characteristics of the simplest halogen containing a* radical: the hydrogen halide radical anion. Hydrogen fluoride, hydrogen chloride, hydrogen bromide and hydrogen iodide radical anions isolated in a variety of host matrices are reported. The large matrix dependence of their magnetic parameters is explained in terms of intermolecular hydrogen bonding to the halogen. Attention is focused on nitrogen-halogen a* radicals in Chapter Four, where they are shown to be radiolytically formed in ammonium halides, mono, di and trialkylammonium iodides and monoalkylammonium bromides. Alkylamanium chloride radicals could not be identified. Chapter Five primarily explores the effect of the halide counter ion on the solid-state radiolysis of some tetraalkylammonium, trialkylsulphonium and trialkylsulphoxonium cations. During the course of the investigation, sulphur-halogen a* radicals are identified in the trialkylsulphonium salts after annealing. The last chapter investigates the factors which determine the type of species formed following electron capture by carbon halogen bonds. Both adducts and a* radicals are characterised and with particular reference to the specific example of iodoacetamide, consideration is given to the factors influencing their stability.

The major target of ionising radiation has been determined as cellular DNA. Damage to DNA, as detected at 77K under conditions of direct damage by ESR, is localised on the bases thymine and guanine. This damage leads to single and double strand breaks, precursors of cell death and mutagenesis. In an attempt to intercept the damage at the bases, before formation of strand breaks, the use of polycations as potential drug delivery systems to DNA has been examined. Magnetic resonance techniques have been used to establish that polyamines used are present almost completely as polyammonium cations at pH 7 and to probe the interactions of a number of polycations with DNA. Sodium-NMR was used to investigate the affinity of polyamines, poly- aminothiols and transition-metal complexes for DNA, via sodium ion displacement from the DNA region. It was found that small metal complexes displace a greater number of sodium ions than polyamines of similar charge. Application of the counterion condensation theory led to a model of the counterions existing within a cylinder around the DNA of approximate radius 20A. The mode of interaction of polyammonium cations was studied using proton magnetic resonance. Linewidths, related to the transverse relaxation rate, give information on the motion of compounds close to DNA. Comparison of linewidths in the presence and absence of DNA revealed no significant broadening. This was interpreted as indicative of a loose, electrostatic interaction, not significantly hindering motion of the cations close to DNA, suggesting rapid motion of polyammonium ions along the DNA. The radioprotection of DNA by various transition-metal complexes was studied using ESR. Certain compounds exhibited protection via electron transfer, resulting in a decreased radical yield.

Radiation Induced effects

No description available.

No description available.

<p> The variation in sensitivity of L60T cells to gamma rays has been studied as a function of position in the cell division cycle. For a dose range of 0-12,000 rads, no significant variation was found for mitotic delay. Such was not the case for sensitivity to cell killing, which was found to increase as the cells passed from G1 through S to G2 of the division cycle. The results of mitotic delay are in disagreement with results published by other workers although the survival data agree with previous reports for a similar cell line. Results reported in connection with cell cycle determinations and mitotic delay suggest that the existence of a repair cycle operating concurrently with the normal cell cycle may be postulated. The theoretical treatment of mitotic delay given by Lea is examined and is not found to describe adequately the present results. Finally, the evidence reported here suggests that mitotic delay and radiation lethality are not separate manifestations of the same phenomenon. Experimental materials for further investigation into the repair processes involved are suggested.</p> / Thesis / Master of Science (MSc)

No description available.

No description available.

Thesis (PhD in AppSc)--University of South Australia, 1996

Diss. (sammanfattning) Stockholm : Karol. inst., 2002. / Härtill 5 uppsatser.