782 RADIATION BIOLOGY 



progress of neuroblasts treated in metaphase, anaphase, or telophase, but 

 retards considerably over half the fibroblasts treated in these stages. 



After doses of radiation, up to and including those barely sufficient to 

 reduce the mid-mitotic count to zero, recovery from the radiation effect is 

 accompanied by a rise of the mid-mitotic count at a rate roughly similar 

 to the rate of fall in the count immediately after treatment, with no pro- 

 longed low count intervening (Fig. 11-5) (Canti and Spear, 1929; Kemp 

 and Juul, 1930; Spear, 1931, 1932, 1935; Wilson et al, 1935; Mottram, 

 1936; Tansley et al, 1937; Lasnitski, 1940; Carlson, 1942; Simon-Reuss 

 and Spear, 1947; Knowlton, Hempelmann, and Hoffman, 1948; Knowl- 

 ton and Hempelmann, 1949; Deufel, 1951). This rise in the mid-mitotic 

 count does not stop at the normal level but continues above it before 

 returning to the normal level. Following very small doses, the rise above 

 the normal after recovery compensates approximately for the fall below 

 normal that precedes it (Fig. 11-5) (Canti and Spear, 1929; Spear, 1931, 

 1932, 1935; Wilson et al., 1935; Tansley et al, 1937; Knowlton and 

 Hempelmann, 1949; Carlson, Snyder, and Hollaender, 1949). From 

 what we know of the behavior of individual cells after treatment, this is 

 exactly what we would expect. In the grasshopper neuroblast, for 

 example, blockage from irradiation affects not only the cells at the most 

 sensitive stages (namely, middle and late prophase) but also cells entering 

 these after treatment in earlier stages, so that an excessively large number 

 of cells accumulates during the period of decreased mitotic activity. A 

 similar increase has been found by Mallet and Perrot (1951) in the 

 Allium root tip. With recovery and the resumption of mitotic progres- 

 sion, these cells will complete mitosis and their numbers should com- 

 pensate exactly for the previous deficit. With larger doses, however, the 

 number of mitoses never exceeds the normal and with still larger doses the 

 return to normal may be greatly prolonged (Alberti and Politzer, 1924; 

 Pekarek, 1927; Canti and Spear, 1929; Kemp and Juul, 1930; Spear, 

 1931, 1935; Tansley et al, 1937; Lasnitski, 1946, 1948; Simon-Reuss and 

 Spear, 1947; Knowlton et al., 1948; Knowlton and Hempelmann, 1949; 

 Carlson et al., 1949). Failure of the mid-mitotic count to surpass the 

 normal is apparently due to the extension of the radiation effect to earlier 

 and earlier stages of the mitotic cycle as the dose is progressively 

 increased, until cells in all stages of the cycle are retarded. 



If the dose is large enough to lower the mid-mitotic count to zero, the 

 larger the dose, the more prolonged is the period of zero activity. Few 

 studies have been made of the relation of the length of this period to 

 dosage, probably because, for most purposes, the investigator has found it 

 more profitable to work with doses that do not completely inhibit mitosis. 

 A dose of 2000 r of y rays reduced the mitotic count of chick fibroblasts 

 in vitro to zero until about 5 hours after treatment (Fig. 11-5). Jungling 

 and Langendorff (1930) reported that in the Vicia root tip mitosis 



