Abstract
Ionising radiation-induced effects in nontargeted bystander cells may play an important role in low-dose cancer risk. Here, we briefly review the experimental systems used for bystander studies, the initiation and intercellular transmission of bystander signals and response mechanisms in recipient cells. Recent evidence that implicates the histone 2A variant X (H2AX) and the deoxyribonucleic acid (DNA) damage kinase ataxia telangiectasia and Rad3-related (ATR) in bystander signalling is highlighted and the implications of bystander responses for human radiation protection are discussed.
Published Version
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