1002 RADIATION BIOLOGY 



rabbit marrow homogenates immediately after X irradiation (Altman 

 et al, 1951) and in fowl erythrocytes after massive exposure (Frankenthal 

 and Back, 1944). While depressed tissue respiration can perhaps be 

 attributed to specific inactivation of oxidative enzymes by the radiation, 

 gross metabolic changes seem to be the result and not the cause of growth 

 inhibition. In fact, effects on growth may occur at dosages considerably 

 below those required to influence metabolism (Hubert, 1929; Fenn and 

 Latchford, 1931-1932 ; Packard, 1933) . The absence of profound changes 

 in the metabolic rate of the whole animal in the presence of possible 

 alteration in endogenous respiration of radiosensitive tissues is not 

 unreasonable, since tissues that account for most of the oxygen consump- 

 tion are notably radioresistant. Tissue breakdown products resulting 

 from irradiation apparently do not result in an appreciable over-all 

 increase in metabolism, perhaps because of their rapid excretion or slow 

 release, the associated inanition, or other as yet unknown factors. 



IMMUNITY AND INFECTION 



It is well known that total-body irradiation decreases resistance to 

 infection and interferes with immune reactions. The action of ionizing 

 radiations on barriers to infection attracted early attention when it was 

 noted that irradiation resulted in a severe depression of leukocytes 

 (Heineke, 1903), inhibition of antibody formation (Benjamin and Sluka, 

 1908; Hektoen, 1915), and a terminal bacteremia of intestinal origin 

 (Stafford L. Warren and Whipple, 1923a; Mottram and Kingsbury, 1924). 

 The development of enterogenous infection in X-irradiated mice, includ- 

 ing some histological evidence of local bacterial invasion of injured 

 intestinal areas, was described subsequently by Chrom (1935), who noted 

 also that bacteremia could be minimized by shielding the liver and spleen 

 during irradiation. The complication of bacteremia was also observed 

 after neutron irradiation (Lawrence and Tennant, 1937). These findings 

 take on added significance in view of the efficacy of antibiotic therapy in 

 certain species (Miller et al, 1950b; Hammond and Miller, 1950; Howland 

 et al, 1950; Furth, Coulter, and Howland, 1951; Koletsky and Christie, 

 1950; Gustafson and Koletsky, 1951) and the effect of spleen shielding 

 on hematopoietic recovery and radiation mortality (Jacobson, Marks, 

 and Lorenz, 1949; Jacobson, Simmons, et al, 1950). 



The problem of radiation-induced infection has been the subject of 

 intensive investigation in recent years, and it now seems clear that 

 enterogenous invasion can be a substantial factor in radiation morbidity 

 and mortality. The cause of the bacteremia still remains a moot ques- 

 tion, however. Miller and co-workers (1950a) have observed that bac- 

 teremia in irradiated mice reaches its apogee during the period of greatest 

 mortality. A somewhat lower incidence of positive blood cultures has 



