IHi: Llll.-Sl'AN OI MITAGENS PR0DUC:ED IN CELLS BY IRRADIATION 



actively mctabolizins; material the oxyu^en tension is only efiective in altering 

 the irradiation damage if present during irradiation. It might be inferred 

 from this that oxygen acts only by increasing the original yield of mutagen 

 at the ionization sites. If this were so it would presumably act as a simple 

 multiplying factor to the dose as has been suggested by Read^^. The con- 

 sistent values of between two and three for the oxygen enhancement men- 

 tioned before seem sulTicient basis for this. However, there is increasing 

 evidence which will be reviewed later, to show that oxygen, not only increases 

 the primary yield of mutagens but by altering the biological protective 

 system and by propagating chain reactions involving the original products 

 also increases the efiective half-life of the mutagens. 



The influence of oxygen on the life-span of mutagens can be demonstrated 

 by changes in the physiological conditions. 



Since the demonstration^^- ^^ that protection against inactivation of 

 enzymes by irradiation can be obtained by relatively small quantities of 

 biological reducing agents such as thiourea, similar protection ])y a range of 

 such agents has been shown in a variety of organisms. Reviews of the 

 literature have been given by Grayl^ Patt^' and Hollaenderi^. Protection 

 against chromosome breakage has been demonstrated by Mikaelsen^^, 

 Riley^o and others. This form of protection operates by limiting the life- 

 span of the mutagenic products and thus differs from the protection obtained 

 by reducing the oxygen concentration. Linked with this is the evidence from 

 numerous experiments which indicates that the final breakage pattern is 

 determined by modification of the results of the initial breakage by oxygen. 

 This is possible either by causing more breakage or by altering the amounts 

 of restitution and reunion between broken chromosome ends. Both these 

 principles have been claimed to be effective. Giles and his co-workers* have 

 advocated the hypothesis of differential breakage while Schwartz-^ and Baker 

 and von Halle'-"- have proposed the differential reunion mechanism. How- 

 ever, it seems that these experiments find a more likely explanation along 

 the general Hnes of an hypothesis suggested by Thoday^^ and Gray-*. This 

 supposes that irradiation causes a spectrum of damage to the chromosomes, 

 producing both actual and potential breaks in proportions altered by ion 

 density and oxygen. The fate of the potential breaks is determined by 

 consequent physiological conditions in which oxygen again plays an 

 important part in transforming latent breaks into actual breaks. 



If oxygen also influences breakage by determining the fate of potential 

 breaks it should be possible to separate experimentally this secondary 

 cumulative effect from the direct effect of irradiation and from the increase 

 to the immediate production of mutagen resulting from the presence of 

 oxygen at the seat of ion formation. In particular, further exploration of 

 these effects is possible by examining the oxygen effect under conditions of 

 dormancy where the enzymes of the jDrotective systems are hardly functional. 

 The irradiation of seed has demonstrated that the oxygen effect is more 

 pronounced in seeds than it is in actively metabolizing tissues. In addition, 

 oxygen alone produces damage similar to that of X-rays. 



Gustafsson^s observed that the frequency of aberrations in the first mitotic 

 divisions in barley after irradiation of the dry seed was doul)led (from 16 

 per cent to 33 per cent) by storage for two months after irradiation. He also 



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