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The many attempts to demonstrate early activation or inactivation of specific enzymes as a consequence of exposure to ionizing radiation in vivo have not succeeded in disclosing the biochem- ical origin of the radiobiological lesion. This failure may be due to localization of the primary bio- chemical events at certain sites within the cell, for in such circumstances the earliest changes might escape detection in studies on whole tissues or homogenates. Such localized intracellular re- sponses have been observed in the behaviour of mitochondrial deoxyribonuclease II (Goutier- Pirotte & Thonnard, 1956) and in the uptake of 32p into liver ribonucleic acid (Payne, Kelly & Entenman, 1952). It seemed likely that in view of the marked disturbance of nuclear function after irradiation, a comparison of the enzymic comple- ment of the nucleus in radio-sensitive (i.e. those tissues which show early histological deterioration after exposure to sublethal radiation) and non- sensitive tissues might provide a clue to the nature of the primary biochemical lesion.
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William A. Creasey (1960) studied this question.
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