QUANTUM rUEOHY OF RADIATION ABSORPTIONS IN TISSUES 1317 



species (76, 97). The analysis of this problem requires rather special 

 material having a broad background of embryological, cytological, and 

 genetic information. The facts of particular experiments can then find 

 their proper place in the interpretations assigned to the experiments. 

 Such material is limited, the best available being Drosophila. 



The physical hypotheses adopted to account for irradiation effect 

 on tissue universally consider the cell as containing a sensitive spot 

 within which the X-ray absorptions are to occur if death is to result. 

 Genetic considerations suggest that this concept be modified to accom- 

 modate the evidence described earlier. The chromatin, as shown by the 

 experiments of Hertwig (41, 42), is the most sensitive material of the cell 

 to irradiation. Radiant energy may affect this material and some of its 

 constituents in various ways. It may cause mutation of the genes to 

 others having different effects, or it may break the connection between 

 genes with the result that the reorganized chromosome has a quite differ- 

 ent constitution from that of the original. It may affect the mechanism 

 of meiosis and result in abnormal germ cells. Different as the effects are, 

 they are all localized in minute space, suggesting the sphere of influence 

 of an electron absorption. Genetic methods show that these effects may 

 be localized within any part of the chromatin. They need not be lethal, 

 although they often alter the genes to make them so. Biologically the 

 sensitive spot of the physical concept becomes many sensitive spots within 

 the chromatin. The reasoning from probability will still apply, however. 



To produce death in the object irradiated it is necessary to injure the 

 cell so that it will no longer function properly in division and develop- 

 ment. This injury would appear to be in the nature of a gene change 

 to convert it into a dominant lethal similar, save for its dominance, to the 

 observed recessive lethals responsible for death in the second generation. 

 This view receives support from the fact that the sex ratios of the progeny 

 of irradiated sperm fertilizing normal .eggs, or of irradiated sperm fertiliz- 

 ing attached X-eggs in Drosophila, behave as they should if such dominant 

 lethals were produced. The effect on the sex ratio in forms like D. 

 obscura having a large X-chromosome is greater thau in forms with a 

 small sex chromosome. This evidence is not completely critical, however, 

 for defects produced in the chromosome framework rather than the genes 

 could account for the result. It is more difficult to account for the follow- 

 ing evidence except by the production of dominant lethal mutations. 

 The sex chromosome of D. melanogaster is known to have one-half to two- 

 thirds of its length empty of genes (26, 78). It is however, possible for 

 this chromosome to break and reattach to another chromosome, the 

 break occurring within the empty (?) region. If we assume that the 

 lethal effects of irradiation are due to chromatin aberrations as against 

 dominant lethal gene mutations, then we would expect that the propor- 

 tion of such abnormalities would be in the ratio of the chromatin in the 



