Abstract
Ionizing radiation is an invaluable diagnostic and treatment tool used in various clinical applications. On the other hand, radiation is a known cytotoxic with a potential DNA damaging and carcinogenic effects. However, the biological effects of low and high linear energy transfer (LET) radiations are considerably more complex than previously thought. In the past decade, evidence has mounted for a novel biological phenomenon termed as "bystander effect" (BE), wherein directly irradiated cells transmit damaging signals to non-irradiated cells thereby inducing a response similar to that of irradiated cells. BE can also be induced in various cells irrespective of the type of radiation, and the BE may be more damaging in the longer term than direct radiation exposure. BE is mediated either through gap-junctions or via soluble factors released by irradiated cells. DNA damage response mechanisms represent a vital line of defense against exogenous and endogenous damage caused by radiation and promote two distinct outcomes: survival and the maintenance of genomic stability. The latter is critical for cancer avoidance. Therefore, efforts to understand and modulate the bystander responses will provide new approaches to cancer therapy and prevention. This review overviews the emerging role of BE of low and high LET radiations on the genomic instability of bystander cells and its possible implications for carcinogenesis.
Highlights
Extensive epidemiological and toxicological research over several decades has focused on the health effects of radiation to understand the risk of exposure to both public and workforce
This study suggested that the initiating events in the cascade that leads to apoptosis induction in nonirradiated cells are by signals produced from the irradiated cells
The general dogma that only direct radiation causes the genomic instability is challenged by the existence of the recent findings of the bystander effect” (BE)
Summary
CT-scans) and RT procedures shows varying health effects in the general population and in cancer patients [8,9,10,11,12,13,14]. In an earlier study it has been reported that the medium collected from the cells exposed to either low or high LET radiations increased the bystander cell survival [23] These studies indicate that the molecules released in the ICM, which further activates the PKC may act as a growth stimulatory effect to the bystander cells. It was noted that the DNA double-strand breaks and apoptotic cell death were induced in bystander mouse cerebellum Accompanying these genetic events, bystander-related tumor induction in the cerebellum of radiosensitive Patched-1 (Ptch1) heterozygous mice after x-ray exposure of the remainder of body, further suggested a mechanism mediated by gap-junctional intercellular communication for transmission of bystander damage to shielded cerebellum. More animal studies will give a concrete evidence of this existing radiation induced bystander phenomenon
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