Bystander apoptosis in human cells mediated by irradiated blood plasma

Vinnikov, Volodymyr; Lloyd, David; Finnon, Paul

doi:10.1016/j.mrfmmm.2011.12.006

Cited by 7 publications

(2 citation statements)

References 54 publications

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“…This is involved in cell-to-cell communications or signaling from the irradiated and unirradiated cells [ 12 , 14 ], and there is no doubt that reactive oxygen species [ 15 ], gap junctions [ 34 , 35 ] and paracrine soluble signals are associated with this pathway [ 13 ]. Furthermore, there are many reports about bystander effects with low energy photon radiation [ 36 , 37 ], while radioactivation is not caused by low energy photon radiation as seen in our results ( Fig 5 ). Due to these differences, we are not proposing that radioactivation can explain major pathways of bystander effects.…”

Section: Discussionsupporting

confidence: 82%

Solution Radioactivated by Hadron Radiation Can Increase Sister Chromatid Exchanges

et al. 2015

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When energetic particles irradiate matter, it becomes activated by nuclear reactions. Radioactivation induced cellular effects are not clearly understood, but it could be a part of bystander effects. This investigation is aimed at understanding the biological effects from radioactivation in solution induced by hadron radiation. Water or phosphate buffered saline was activated by being exposed to hadron radiation including protons, carbon- and iron-ions. 1 mL of radioactivated solution was transferred to flasks with Chinese hamster ovary (CHO) cells cultured in 5 mL of complete media. The induction of sister chromatid exchanges (SCE) was used to observe any increase in DNA damage responses. The energy spectrum and the half-lives of the radioactivation were analyzed by NaI scintillation detector in order to identify generated radionuclides. In the radioactivated solution, 511 keV gamma-rays were observed, and their half-lives were approximately 2 min, 10 min, and 20 min. They respectively correspond to the beta+ decay of 15O, 13N, and 11C. The SCE frequencies in CHO cells increased depending on the amount of radioactivation in the solution. These were suppressed with a 2-hour delayed solution transfer or pretreatment with dimethyl sulfoxide (DMSO). Our results suggest that the SCE induction by radioactivated solution was mediated by free radicals produced by the annihilated gamma-rays. Since the SCE induction and DMSO modulation are also reported in radiation-induced bystander effects, our results imply that radioactivation of the solution may have some contribution to the bystander effects from hadron radiation. Further investigations are required to assess if radioactivation effects would attribute an additional level of cancer risk of the hadron radiation therapy itself.

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Section: Discussionsupporting

confidence: 82%

Solution Radioactivated by Hadron Radiation Can Increase Sister Chromatid Exchanges

et al. 2015

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“…Supported by other observations, this phenomenon was later termed the radiation-induced bystander effect (RIBE), which is defined as physiological changes in unirradiated cells manifested by cells exposed to radiation ( Sokolov et al, 2005 , 2007 ; Klammer et al, 2013 ). Apart from SCE, various biological consequences of RIBE have been observed in different studies such as genomic instability, micronuclei formation, apoptosis, micro RNA (miRNA) regulation, and differentiation ( Lorimore et al, 1998 ; Belyakov et al, 2002 ; Kovalchuk et al, 2010 ; Vinnikov et al, 2012 ). A common feature of RIBE seems to be induction of DNA damage.…”

Section: The Bystander Responsementioning

confidence: 99%

Bystander communication and cell cycle decisions after DNA damage

Jaiswal

Lindqvist

2015

Front. Genet.

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The DNA damage response (DDR) has two main goals, to repair the damaged DNA and to communicate the presence of damaged DNA. This communication allows the adaptation of cellular behavior to minimize the risk associated with DNA damage. In particular, cell cycle progression must be adapted after a DNA-damaging insult, and cells either pause or terminally exit the cell cycle during a DDR. As cells can accumulate mutations after a DDR due to error-prone DNA repair, terminal cell cycle exit may prevent malignant transformation. The tumor suppressor p53 plays a key role in promoting terminal cell cycle exit. Interestingly, p53 has been implicated in communication of a stress response to surrounding cells, known as the bystander response. Recently, surrounding cells have also been shown to affect the damaged cell, suggesting the presence of intercellular feedback loops. How such feedback may affect terminal cell cycle exit remains unclear, but its presence calls for caution in evaluating cellular outcome without controlling the cellular surrounding. In addition, such feedback may contribute to how the cellular environment affects malignant transformation after DNA damage.

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