THi: i.iii.-si'A.N oi- ML r.u.KNs i'R( )DLc;i:i) IN c;i:lls ijv ikradiaiiox 



The continued increase in lireakatije during the first 10 days following 

 irradiation has important implications. It demonstiates conclusively that 

 either mutagenic substances having a long half-life are able to exist after 

 irradiation, or that some auto-j)ropagative reactions, which are al:)le to 

 supplv these compounds, are set in motion by the irradiation. Either or both 

 these conditions are of course possible. Since these processes require oxygen 

 it seems likely that they are similar to the mechanisms already proposed by 

 Weiss^s^ Readi2-i3, and Gray^^. 



The leaching experiments indicate that the presence of such mutagenic 

 substances can be demonstrated directly by this method. If these active 

 compounds can be identified with the irradiation-oxygen interaction then it 

 seems that leaching may provide a method of isolating the active compounds(c/'. 

 ScarasciaandScarascia-Venezian'^-'andD'AmatoandHofTmann-Ostenhof'*'). 



If post-irradiation effects occur in states of metabolic rest it is likely that 

 they also operate to a limited extent in states of unrest. The only suppressing 

 influences here are active protective systems and if these are temporarily 

 saturated or inactivated by the irradiation there seems no reason why delayed 

 breakage should not be important in general. This immediately raises the 

 question as to whether the oxygen eflfect is not merely the expression of this 

 continued form of breakage. Such an effect would explain the mechanisms 

 of latent breaks advanced by Thoday"*^, Gray^^, Liining*^ and Swanson^. 

 This continued opening of latent breaks due to the prolonged production of 

 mutagen could conceivably account for the so-called 'open period' and its 

 dependence on dose and metabolic rate. The correlation between breakage 

 and delay in reunion at dififerent oxygen tensions would be explained. The 

 life-span of these mutagenic substances or their continued production would 

 depend upon factors modifying the metabolic rate. In anoxic conditions the 

 production of mutagens is limited because in low oxygen concentrations the 

 balance of the reactions shifts away from the production of peroxy com- 

 pounds. A similar reduction in the effect would be obtained if the active 

 oxidative mutagens are removed by suitable reducing agents such as cysteine. 

 These agents would decrease the apparent mean free path of the mutagens. 

 On the other hand, if the enzyme systems removing these oxidative products 

 are inhibited by carbon monoxide or other metabolic poisons, then the life 

 span of these radiation products is increased. From this it will be seen that 

 the results of the fractionation and intensity experiments using reducing 

 agents such as BAL, and metabolic inhibitors such as carbon monoxide, can 

 be explained by continued breakage. While the argument that the reunion 

 process is dependent on the metabolic rate is sound, and it is certain that 

 reunion accounts for some of the oxygen effect, it seems likely that most of 

 the oxygen effect is attributable to delayed breakage. It is certain that 

 reunion cannot explain the increased breakage in post-storage experiments. 



CONCLUSIONS 



An analysis of chromosome breakage in Allium cepa after treatment of the 

 dry seed by doses of 1 -2 kr of X irradiation combined with pre- and post- 

 irradiation storage shows the following: 



(7) oxygen appears to be a most important factor in the process of ageing. 

 Chromosome breakage increases exponentially with storage time in air, 



206 



