Abstract

Health risks to human and non-human biota exposed to low dose ionising radiation remain ambiguous. The need to establish risk assessment standards based on the mechanisms underlying low level radiation exposure has been recognised by regulatory agencies as critical to adequately protect people and to make the most effective use of national resources. Both gap-junction intercellular communication and oxidative metabolism have been shown to mediate 'adaptive' and 'bystander' effects in mammalian cells exposed in vitro to low dose/low fluence ionising radiation. While adaptive responses are thought to mitigate the harmful effects of radiation, bystander effects have been suggested to amplify its consequences. The exact molecular steps by which adaptive and bystander effects are elicited have not been defined. Here we discuss a few of the molecular and biochemical events underlying these effects. Our data indicate that dose, dose-rate, and the linear energy transfer of the radiation are critical in inducing the changes that determine whether protective or harmful effects are expressed at low dose/low fluence ionising radiation.

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