Radioprotection by DMSO of mammalian cells exposed to X-rays and to heavy charged-particle beams

Abstract

Populations of G1-phase Chinese hamster cells in stirred suspensions containing various concentrations of DMSO were irradiated with 250 kV X-rays or various heavy charged-particle beams. Chemical radioprotection of cell inactivation was observed for all LET values studied. When cell survival data were resolved into linear and quadratic components, the extent and concentration dependence of DMSO protection were found to be different for the two mechanisms. The chemical kinetics of radioprotection for single-events were similar for LET values up to those which gave the maximum RBE. DMSO protected to a lesser extent against energetic argon ions at an median LET of approximately 220 keV/micron. These data could indicate the contribution of indirect action by hydroxyl radicals and hydrogen atoms to cell inactivation by single-hit and double-hit mechanisms for various radiation qualities. The decrease in RBE observed at very high LET may result, in part, from reduced yields of water radicals at 10(-9)-10(-8) s resulting from radical recombination mechanisms within the charged particle tracks.

Heavy-Ion Radiobiology: Cellular Studies

“…Using particle beams of H 2 +, Li3+, c 6 +, Ne 10 +, and Ar 18 + of initial energies from 8.5 to 570 MeV/u, Roots et al (198Gb, 1981) found that the contribution to cell killing by hydroxyl radicals was highly dependent on particle velocity and atomic number, but that the results did not correlate well with LEToo for the high energy particles. Although, in general, the fraction of the total radiation damage caused by hydroxyl radicals decreased with increasing LET as has also been shown by others (Brustad, 1962;Manney et al, 1963;Takeshita and Sawada, 1974;Singh et al, 1976;Chapman et al, 1979). In ~he case of the low energy particle beams where fragmentation is minimal, the decrease in the extent of hydroxyl-radical induced cell lethality with respect to LET, corresponded to the decrease in G(OH) values from Vereschinskii and Pikaev (1964) as a function of LET.…”

“…10. Combined application of drugs~ hyperthermia, anisotonic solutions, time delay, and radiations including sequential treatments of heavy ions and X rays (Chapman et al, 1977(Chapman et al, , 1978(Chapman et al, , 1979Gerner and Leith, 1977;Guichard et al, 1982;Ngo et al, 1981;Roots et al, 1982;Schroy et al, 1980b;Tenforde et al, 1981bTenforde et al, , 1982b). …”

“…Studies of the cellular inactivation by charged particle beams and the radioprotection afforded by dimethyl sulfoxide (DMSO) have also been examined (Chapman et al, 1979). Interest in these studies stems from the fact that the extent and concentration range for DMSO protection of single and double event mechanisms of x ray inactivation (using the linear-quadratic model) have been shown to be qualitatively and quantitatively different from each other (Reuvers et al, 1973).…”

“…Interest in these studies stems from the fact that the extent and concentration range for DMSO protection of single and double event mechanisms of x ray inactivation (using the linear-quadratic model) have been shown to be qualitatively and quantitatively different from each other (Reuvers et al, 1973). Since the radioprotection by OMSO has been attributed to its ability to scavenge hydroxyl radicals generated by radiation in the vicinity of cellular targets, Chapman et al (1979) have attempted to titrate the relative hydroxyl radical concentration produced at lo-9 sec in various charged particle tracks. Use of the Bevalac beams for this purpose is somewhat complicated by the presence of a wide distribution of ionization densities which result from the primary and secondary particles, as well as low LET delta-rays.…”

Chemical agents that promote chromatin compaction radiosensitize tumour cells

“…The indirect eVect of hydroxyl radicals is known to play unlike the more localized expression of phosphorylated H3. These data represent our rst attempts a major role (~85%) in cell killing by the single-hit mechanism (Chapman et al 1979, Chapman 1980. to quantify molecular factors that are uniquely expressed when chromatin is compacted for And when chromatin is compacted, the probability of producing multiply damaged, irreparable lesions correlation with increased radiation sensitivity.…”