ANTIMITOTIC ACTIONS 535 



were formed in the cells. It would be important to know if such reactions 

 apply to the conjugates of the quinones with cysteine or glutathione. 

 This theory does not very well explain the relative inactivities of Compounds 

 I, II, and VI. 



Relatively little attention has been given to the possibility that the 

 hydrogen peroxide formed during the oxidation of the hydroquinones is 

 at least partly responsible for the mitotic inhibition. Dold et al. (1963) 

 pointed out that hydrogen peroxide is formed particularly in glycolyzing 

 cells such as the Ehrlich ascites carcinoma and felt that it is a primary 

 factor in the effects of 9,10-phenanthrahydroquinone, while Kayser (1964) 

 suggested that autoxidation of this substance produces enough hydrogen 

 peroxide to account for the effects, and showed that 0.0025 vaM 9,10- 

 phenanthrahydroquinone depresses glycolysis 92% if the incubation is 

 aerobic but has no effect under anaerobic conditions. Catalase is also able 

 to protect the cells. 



Radiosensitizing Action 



Certain quinones potentiate the antimitotic action of X-irradiation on 

 fibroblasts and for this reason have been termed "radiosensitizers" (Mit- 

 chell and Simon-Reuss, 1947, 1952 a). This action could well be an important 

 one in the clinical use of the quinones in tumor therapy. Menadiol-diP 

 has been especially studied in this respect and the results shown in the 

 accompanying tabulation are typical. The inhibition with the combined 



treatment is much greater than would be expected if the individual effects 

 were additive.* These results indicate that the mechanisms in the two 



* The % inhibitions are not to be summed even though the actions are additive. 

 In the first experiment the predicted inhibition from combined treatment would be 

 around 46% and in the second experiment around 68%, so that the experimental 

 results give inhibitions 36-38% greater than expected. 



