MAMMALIAN RADIATION GENETICS 145 



More recently, additional attempts have been made to detect an over-all effect on 

 viability. Boche et a/. 113 reported on the life expectancy of the progeny of irradiated 

 male and female mice, as measured from the time of weaning. Their controls con- 

 sisted of litters sired prior to irradiation and the experimentals were produced at three 

 intervals of time after irradiation: 10 days, 120 days, and 180 days. The study was 

 done in two replications; the first indicated a shorter life expectancy among the experi- 

 mentals, the second was negative. The use of controls of a different parity than any 

 of the experimental groups is not to be recommended. Litter size and maternal 

 nutritional factors will be confounded with any induced genetic effects of the radiation. 



Russell 1133 reported a significant shortening of life among progeny of irradiated 

 males for mice conceived during the presterile period. The offspring had their mean 

 life expectancy from weaning reduced by about 60 days per 100 rep exposure of the 

 male parent. This is generally considered to be a maximum effect, since the parents 

 were subject to a prompt neutron exposure from a nuclear weapon detonation and the 

 progeny were conceived from cells in postgonial stages at irradiation. The mutation 

 rate for these stages is twice that for spermatogonia and the n:x RBE may lie any- 

 where between 2 and 6. Russell and Russell 1137 have indicated that follow-up studies 

 employing X irradiation of spermatogonia confirm the earlier report on neutron effects 

 but the expression is less readily detected. 



Preweaning mortality in mice has been measured as a reduction of litter size at 

 three weeks of age. 1137 Litters produced from germ cells exposed in the spermatogonial 

 stage show a 3 to 4 per cent reduction from control values following a 300 r, X-ray 

 exposure. No information on the time of death of the animals during the three-week 

 period was given. Total infant mortality, including stillbirths, has recently been 

 studied in rats with the suggestion that some part of the mortality is genetically caused 

 rather than a random function of maternal and litter-size factors. 824 The technique 

 consisted of a comparison of control and experimental litters of similar size for differences 

 in postnatal mortality, rather than a comparison of litter sizes themselves, since progeny 

 were produced dui^ig the presterile period and the litter sizes reflected dominant 

 lethal effects occurring prenatally. 



Of the studies reported to date, none has really obtained the data required to 

 provide an accurate and quantitative assessment of the full expression of viability 

 mutations. It is imperative that studies be done with the view of encompassing the 

 whole life table; populations must be studied from birth through death as a unit 

 experiment. It is especially important that careful attention be given to the period of 

 neonatal and infant mortality because of the significance of such data for comparison 

 to man. 



It is further suggested that the analysis of data for viability be done by standard 

 methods of actuarial statistics. These are amply described by Pearl. 995 Surprisingly, 

 complete life tables have apparently never been obtained for populations of laboratory 

 mammals. The author is presently endeavoring to accumulate a sufficient number of 

 mouse days of experience to generate the tables for about a half-dozen standard 



