ETHYL METHANE SULPHONATE 261 



The difference between 693 days for the EMS treated and 762 for the control 

 is not statistically significant. Furthermore, the true value for the life-span in 

 the EMS group would be some days longer since many of the mice in this 

 group were kiUed when in a moribund state because we wished to examine 

 them histologically. We found that the EMS-treated group developed a high 

 mcidence of hmg and kidney tumours. The latent period for this carcinogenic 

 action of EMS woidd appear to be so long that it had no appreciable influence 

 on life-span. 



Table I 



t The radiation and the chemicals were administered to 11-14-week-old animals at three 

 weekly intervals. 



X Time when 50% of the mice were dead. 



§ Most of the animals in this series were killed when they reached a moribund state to assist 

 pathological study. The true Mfe-span of the animals that had received ethyl methane sul- 

 phonate is therefore longer and approximates more closely to that of the controls. 



While we have no direct data showing the relative number of somatic 

 mutations produced in the mouse by the treatments tested in Table I, 

 figures are available (see Table II) for the production of sex-linked recessive 

 lethal mutations in DrosojjJiila. If, for purposes of comparison, we equate mice 

 with Drosopliila then it can be seen from Table II that the EMS treatment used 

 in the mice (i.e. as shown in Table I) provokes very many more mutations 

 than do the treatments with X-rays, myleran and chlorambucil. Though on a 

 weight basis these chemicals do not differ very greatly in mutagenicity, in 

 mice the EMS treatment is likely to be much more mutagenic than the others 

 because this substance could be administered at much higher doses. 



While the extrapolation from germ mutations in the fruit-fly to somatic 

 mutations in the mouse involves many uncertainties, the difference in the 



