MANNER OF PRODUCTION OF MUTATIONS 563 



about 1200 r. The reaction is not in any part prevented by posttreat- 

 ment with light. Since it is extremely unlikely that enough breaks occur 

 normally to give this frequency of aberrations when the joining of their 

 ends is interfered with, it seems clear that this effect of oxygen at least is 

 on the breakage process. Moreover, it is noteworthy that the effect of 

 the oxygen was nearly doubled when a dose of only 2 r of 7 rays was 

 applied at the same time, i.e., there seems to be a synergism of the effects 

 of the oxygen and of the ionizing radiation. Nevertheless, the mutagenic 

 pathways of these two agents must in this case differ considerably since 

 in their latest work Conger and Fairchild (1952b) find that temperature, 

 and also moisture, influence the effects of the two agents differently. It 

 is concluded that this mutagenic action of oxygen by itself is indirect, 

 i.e., via metabolic processes. The question why the chromosomes 

 of this particular material are broken so readily by mere oxygen is obvi- 

 ously an involved chemical one that demands detailed knowledge of the 

 enzymes and other protoplasmic materials present. At the same time, 

 the fact that light does not counteract the effect suggests that the pres- 

 ence of inactive cytochrome does not explain the problem since this 

 oxidase tends to be activated by light. 



Not only the frequency of chromosome aberrations but also that of 

 phenotypically recognizable mutations, most of them probably point 

 mutations, is increased by the influence of oxygen present during expo- 

 sure to ionizing radiation. Thus, D'Amato and Gustafsson (1948) noted 

 an increase in the frequency of visible mutations induced by X rays in 

 barley seeds when hydrogen peroxide was added to the water in which 

 the seeds were soaked before irradiation. Ozone applied to Drosophila 

 males during X irradiation, or by itself, caused no detectable increase in 

 the frequency of lethals induced (Telfer and Muller, 1950, unpublished 

 data), but, since ozone is highly toxic, it was probably impossible to give 

 a sufficient dose. Baker and Sgourakis (1949, 1950), on the other hand, 

 found that Drosophila males exposed to X rays in ordinary oxygen pro- 

 duced offspring with decidedly more lethals (about 40-70 per cent more) 

 than males exposed to X rays in nitrogen. This was true even at the 

 relatively low dose of 1000 r, where few of the lethals are associated with 

 chromosomal changes. By analogy, these results on gene mutations 

 would support the view that breakage rather than restitution is the 

 process affected by oxygen in its influence on chromosome aberrations. 

 In later work. Baker and Edington (cited by Hollaender, Baker, and 

 Anderson, 1952) found that the curve relating lethal frequency to oxygen 

 concentration in Drosophila is similar to the curves for chromosome 

 changes and the mitotic inhibition, which have already been discussed, in 

 showing a decided bend toward the horizontal as the pressure of oxygen 

 in air is approached. This is again an indication that all these effects 

 stem in common from a given type of change in the protoplasmic fluid. 



