1066 



RADIATION BIOLOGY 



The mechanism whereby phenylhydrazine-induced anemia or phlebot- 

 omy reduces the inhibition of erythropoiesis expected after a given dose of 

 X radiation is probably unrelated to the observation of Dowdy, Bennett, 

 and Chastain (1950) in which survival of rats exposed to lethal doses of 

 X radiation was enhanced by reducing oxygen tension available to the 

 animals to about 6 per cent during irradiation. This latter procedure, 



Ht 





4B 





w 



4C 



Fig. 16-17. The effect of 800 r of total-body roentgen irradiation on normal and 

 hyperplastic bone marrow of the rabbit. (IA,B,C) Range of normal control marrow. 

 (2A,B,C) Bone marrow after phenylhydrazine-induced hyperplasia, 3, 4, and 6 days, 

 respectively, after phenylhydrazine withdrawal. (3A,J3,C) Bone marrow of phenyl- 

 hydrazine-induced hyperplasia at 1, 3, and 5 days, respectively, after 800 r and 3, 4, 

 and 6 days, respectively, after phenylhydrazine withdrawal. (AA,B,C) Bone marrow 

 of normal rabbits exposed to 800 r at 1, 3, and 5 days after 800 r. Magnification 16 X. 

 (Originally published in Science, 107: 248, 1948.) 



for all practical purposes, stops metabolic activity, whereas phenyl- 

 hydrazine or phlebotomy actually enhances the metabolic activity of the 

 cells concerned in erythropoiesis. The mechanism whereby phenyl- 

 hydrazine- or phlebotomy-induced hyperplasia reduces the expected 

 radiation effect is not known, but it must be assumed that some metabolic 

 change within the cells renders them less susceptible to radiation. 



Use of Estrogens. Treadwell, Gardner, and Lawrence (1943) demon- 

 strated that estradiol benzoate, given 10 days prior to X radiation in the 



