262 PETER ALEXANDER AND MISS D. I. CONNELL 



observed mutation yield in Drosophila between EMS and the other treat- 

 ments is so great that one can feel confident that the same relative order is 

 maintained. A possible objection is, that in the body of the mouse, EMS is 

 distributed differently from myleran and chlorambucil and that the cells of 

 certain organs are not exposed to the mutagenic action of EMS while the 

 other chemicals— and of course X-rays— reach them. Investigations (Roberts 

 and Warwick, 1958) concerning the metabolic fate of myleran and EMS make 



Table II. Mutagenicity of different treatments in Drosophila 



t Values taken from data by Fahmy and Fahmy (1961). 



X Values computed on the assumption of a linear dose-response curve and assuming one 

 fly weighs 1 mg. 



such differences seem imlikely and more recent studies by Drs. J. J. Roberts 

 and G. P. Warwick (impubHshed) with i^C-lal^elled EMS, myleran and nitro- 

 gen mustard have shown that in the rat these substances are quickly dispersed 

 all over the body and that by 1 hour after administration there is no evidence 

 of any localization. At later periods the radioactivity is highest in the excre- 

 tory organs because of the elimination of metabolites, but even in this respect 

 all the compounds behave similarly. 



We conclude from these experiments that the induction of somatic 

 mutations is not responsible for the life-span shortening in mice induced by 

 X-rays and the bifunctional radiomimetic alkylating agents used by us, since 

 a treatment with EMS which probably produces many more mutations does 

 not shorten life-span. The available data is consistent with the hyi)othesis 

 (see Alexander and Connell, 1960) that the observed effect on life-span by 

 X-rays and the bifunctional alkylating agents is a result of their cell-killing 

 action— immediate or delayed— since EMS has virtually no effect on dividing 

 cells. 



