Abstract

Studies on radiosensitization by oxygen and radioprotection by sulfhydryl-containing compounds have often directed attention to the importance of interactions of those two agents — oxygen and thiols — in determining radiation response. The so-called repair-fixation theory suggests radiation response is determined by a competition between damage fixation by oxidizing agents (e.g., oxygen) and damage repair by reducing species (e.g., sulfhydryls) 1,2: Open image in new window Open image in new window where T· represents an ionizing radiation-induced organic radical on a cellular “target” molecule, TH, such as DNA, and RSH is any thiol. This competition can be clearly demonstrated in simple chemical systems and in nucleic acids such as poly(A) and transforming DNA, and it has been shown that the damage fixation reaction is over 100 times faster than the H donation, chemical repair reaction (reviewed recently3). But the occurrence of this competition in mammalian cells is more difficult to demonstrate. This paper will review the current literature indicating the involvement of this chemical competition in determining radiation response in mammalian cells.

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