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There emerged an upsurge of concern on the diverse cellular response to radiation which was new to the existing paradigm of radiobiology. They include adaptive response, genomic instability, bystander effect, pseudocytokine effect and apoptosis. Their molecular mechanism and health consequences are largely unknown. However, accumulated data indicate that they are all cellular manifestations of programmed adaptive mechanism intrinsic to the organisms for the existence of life either by epistatic response to minimize the negative impact (adaptive response) or by remodeling their genome (genomic instability). The cells have efficient damage sensing and signaling mechanisms for dose-dependent blanching cooperated by protein kinase C (PKC), p38 mitogen-activated protein kinase (p38MAPK) and phospholipase C (PLC) with p53 protein as a downstream effector. The signals are transferred to the bystander cells for orchestrated response. For the adaptive response to have an effect in vivo, two hits must be present within a limited time in a cell or a mass of bystander cells. This determines a minimum effective dose rate, below which remodeling of genome in tissue by apoptotic removal of cells with potentially genotoxic damage may be the prevailing mechanism for modulating radiation effect. Dose refractoriness of chromosome aberrations of stem cell origin in human low dose-rate exposures is consistent with this model. |
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