1080 RADIATION BIOLOGY 



approach, found that cysteine and spleen shielding similarly had an 

 additive effect on survival of mice exposed to X radiation. Furthermore, 

 it was found that, when the techniques of pretreatment with estrogens 

 and cysteine and spleen shielding during irradiation were all combined, 

 an additive effect on survival was observed (Bethard, Simmons, and 

 Jacobson, 1951). Jacobson (1952) found that pretreatment with 

 cysteine followed by 1025 r of total-body X irradiation and postirradia- 

 tion intraperitoneal transplantation of normal spleen were also additive 

 in enhancing survival. Cysteine fails to produce any enhancing effect on 

 survival of irradiated mice when given after 1100 r of total-body X 

 irradiation whether or not the mice had spleen shielding during irradiation 

 (Jacobson, 1952). These studies, although interesting, shed no light on 

 the obvious question of whether or not the pretreatment or prophylactic 

 techniques are related to the therapeutic techniques from the standpoint 

 of mechanism. 



ANTIBODY-FORMATION STUDIES 



The fact that a single total-body exposure to X rays inhibits antibody 

 formation is well documented (Benjamin and Sluka, 1908; Hektoen, 

 1918). The time of antigen injection relative to irradiation determines 

 to a large measure the degree of inhibition (Benjamin and Sluka, 1908; 

 Hektoen, 1918). Exposure of rabbits to dosages of total-body X irradia- 

 tion ranging from 250-800 r effectively suppresses the development of 

 appreciable antibody titer of particulate antigens administered in the 

 24 hours before or the 48 hours after irradiation (Benjamin and Sluka, 

 1908; Hektoen, 1918). It would appear from these observations that 

 irradiation either destroys the cells concerned with antibody formation or 

 reduces their functional capacity to react in the normal way to the 

 injected antigen. It is not known with certainty in which cells of the 

 body this function normally resides, but it has been postulated in a 

 broad sense that the cells of the reticuloendothelial system are responsible. 

 As suggested by Hektoen (1915) the degree of inhibition of antibody 

 formation correlates well with the extent of damage to the blood-forming 

 tissue induced by irradiation. 



It has been demonstrated by Jacobson, Robson, and Marks (1950) that, 

 if the spleen or the appendix of the rabbit is surgically exteriorized and 

 shielded with lead during total-body exposure to 800 r, the capacity to 

 form antibodies to a particulate antigen injected 24 hours after irradiation 

 is retained. In another series of experiments this observation was carried 

 a step further (Jacobson and Robson, 1952). Spleen-shielded rabbits 

 were exposed to dosages of 800 or 500 r of total-body X irradiation. 

 Twenty-four hours later the spleen was removed surgically. After 

 another 24-hour period (48 hours after irradiation) a particulate antigen 

 (sheep red cells) was given intravenously. The capacity of these animals 



