PHYSIOLOGY OF RADIATION INJURY 987 



Bunting, 1932; Ely, Ross, and Gay, 1947; Rhoades, 1948a). This may 

 be attributed, in part, to the phenomenal regenerative capacity of liver 

 cells, and possibly to the low oxygen tension of the tissue. In an early 

 study, Seldin (1904) compared irradiated and shielded areas of the same 

 liver and was unable to detect any difference. The results of an extensive 

 investigation reported by Rhoades (1948a), in which the livers of rabbits, 

 rats, mice, and guinea pigs were examined after total-body X irradiation 

 with dosages of 25 to 1200 r confirm the radioresistance of liver epi- 

 thelium. Alterations, when observed, are considered to be secondary to 

 the general toxicity. When irradiation is accomplished with internal 

 emitters, histological change is also minor, with the notable exception of 

 plutonium, in which case hepatic injury is an outstanding feature of the 

 poisoning (Brues, 1948). 



A nonspecific fatty infiltration is sometimes seen in the livers of irradi- 

 ated animals. The appearance of sudanophile fat in the mouse liver has 

 been attributed to the release of histamine-like tissue breakdown products 

 (Ellinger, 1945). Liver cholesterol has been shown to decrease and liver 

 glycogen to increase during the first two days after total-body irradiation 

 (North and Nims, 1949). These changes may reflect an increased 

 adrenal cortical activity. After local irradiation of the hepatic area of 

 the guinea pig, glycogen disappears somewhat more slowly from the liver 

 upon incubation (Ullmann, 1933). Inhibition of glycogen cleavage is 

 greater with 1200 r than with 600 r but is not well correlated with the 

 changes in total liver glycogen. 



The possibility of metabolic disturbances in the liver that are not 

 manifested by morphological alterations is indicated by the decrease in 

 oxidative capacity of surviving liver slices obtained from animals exposed 

 to 7 and X rays or a rays from injected plutonium (Barron, 1946; DuBois, 

 unpublished observations, 1950). It is of interest that the oxidations 

 that are inhibited are those normally catalyzed by sulfhydryl enzymes. 

 However, it is noteworthy that other sulfhydryl enzymes in the liver are 

 not inhibited by large dosages of ionizing radiation. Thus there are no 

 significant changes in succinic dehydrogenase and adenosine triphos- 

 phatase when specific assays for these enzymes are made on livers taken 

 from mice exposed to y rays (DuBois, Cochran, and Doull, 1951a). The 

 activity and distribution of non-mercapto enzymes (catalase, alkaline 

 phosphatase, esterase, arginase, and rhodanase) in liver cells and in liver 

 connective tissue are unchanged following irradiation with 500 r (Ludewig 

 and Chanutin, 1950b). After lethal dosages, liver catalase activity is 

 decreased (Feinstein et al., 1950), while alkaline phosphatase is increased 

 (DuBois, unpublished observations, 1950). 



Impairment of oxidative mechanisms, as well as possible changes in 

 phosphatase activity, may account for the decrease in acid-soluble 

 organic phosphorus, the increase in inorganic phosphorus, and the 



