The Role of Oxygen-Derived Free Radicals in Radiation-Induced Damage and Death of Nondividing Eucaryotic Cells

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Abstract
Isolated rat alveolar macrophages were exposed in vitro to varying doses of X-radiation. Using dye exclusion as a test for viability, these macrophages were quite radioresistant relative to other eucaryotic cells. A dose of 11,500 rad was required to kill 50% of the cells when viability was assessed 24 h after irradiation. Superoxide dismutase, catalase and diethylenetriaminepentaacetic acid (DETAPAC) gave significant protection; ethylenediaminetetraacetic acid and mannitol showed little or no protection by scanning electron microscopy. A characteristic function of these cells was measured following exposure to radiation in the absence and presence of the putative protection agents. Phagocytic function, assessed by the rate of ingestion of killed yeast particles, was measured before and after exposure of a population of pulmonary macrophages to 2805 rad. This dose of radiation caused a 75% loss of phagocytic function in the irradiated cells. DETAPAC when present during irradiation of the pulmonary macrophages provided nearly complete protection against loss of function. Pulmonary macrophages incubated under specific conditions with superoxide dismutase and catalase retained 50% of the activity of nonirradiated cells. Hydroxyl radicals generated from superoxide anions, H2O2 and Fe apparently are the agents of O2-induced cell damage caused by ionizing radiaton.