ARSINE 793 



that essentially all the arsine is taken up by the erythrocytes and later 

 released in the form of arsenite to the other tissues, but Hughes and Levvy 

 showed that other tissues contain arsenite before hemolysis occurs, so that 

 some of the effects may be due to a direct action on the metabolism of the 

 tissues. These effects probably vary with the rate of administration of arsine; 

 if the amount exceeds that which the erythrocytes can bind, some will 

 enter and directly affect the tissues. 



It has been shown that various thiols and dithiols can fairly well pre- 

 vent the hemolysis caused by arsine, as well as the respiratory depression 

 in tissue slices (Kensler et al., 1946). When arsine is 0.19% in the gas phase, 

 kidney slice respiration is inhibited around 60-70%. The inhibition develops 

 slowly, none being observed during the first hour (the values in the tab- 

 ulation above were obtained during the third hour), which points to the 

 action of some metabolic product of arsine. Dimercaprol has been claimed 

 to be effective in protecting animals from arsine (Kensler et al., 1946), 

 but its clinical use in poisoning has been disappointing (McKinstry and 

 Hickes, 1957). In those cases in which dimercaprol is effective, as in respir- 

 atory inhibition in vitro, one must assume that some intermediary product 

 from arsine reacts with the dithiol, perhaps an early oxidation product 

 such as hydroxyarsine, although some of the antagonism may be through 

 an inactivation of the arsenite eventually formed. The mechanism by 

 which arsine directly alters tissue metabolism are undoubtedly complex 

 and it is doubtful if they will be delineated until more extensive study 

 has been made of the products formed from arsine and their effects on 

 various enzymes and metabolic pathways. 



