312 Z. M. BACQ AND P. ALEXANDER 



tively proposed that this behaviour could be explained either by the 

 HO2 radical hypothesis (Alexander, 1953; Alexander et al., 1955) or by 

 reaction with an organic radical (Alexander and Charlesby, 1955a) in 

 which repair by the protector and irreversiljle damage by oxygen 

 addition could l)e considered as opposing processes. Possibly in the 

 absence of oxygen, the radical R° may undergo spontaneous rej^air by 

 other cell constituents, and added chemicals do not then protect. In 

 the presence of oxygen the radical R° becomes peroxidized unless there 

 is a protective agent present which prevents this reaction and thereby 

 protects against that part of radiation injury that requires oxygen. 



In the last five years chemical investigations (cf. Bacq and Alexander, 

 1955) have made it less likely that HO2 radicals (formed in water by 

 H + O2) are chiefly responsible for cell damage and this is why we have 

 shifted our emphasis to the repair mechanism. However, either process 

 requires that cysteamine protects as a result of reacting with a free 

 radical. 



ACKNOWLEDGMENTS 



This investigation has been supported in Belgimn by gi'ants of the Ministere 

 de rinterieur and of the Institut Intei'universitaire des Sciences nucleaires, in 

 Great Britain by grants to the Cliester Beatty Research Institute (Institute of 

 Cancer Research, Royal Cancer Hospital) from the Medical Research Council, 

 the British Empire Cancer Campaign, the Jane Coffin Childs Memorial Fund 

 for Medical Research, the Anjia Fuller Fund, and the National Cancer Institute 

 of the National Institutes of Health, U.S. Public Health Service. 



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