Cytogenetic adaptive response in cultured human lymphocytes: dependence on the time of exposure to adapting and challenging doses of γ-rays

Ryabchenko, N.I.; Antoshchina, M.M.; Fesenko, E.V.; Иванова, Т. И.; Kondrashova, Tatiana V.; Nasonova, Valentina A.

doi:10.1016/s1383-5718(98)00102-8

Cited by 20 publications

(2 citation statements)

References 27 publications

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“…For each donor, the expected frequencies of MN in combined treatments (AD + CD) were calculated as the sum of the MN in two individual treatments minus the frequency in untreated control cells, as in our earlier publications and also in the great majority of AR investigations [31, 32]. The statistical significance of the observed frequencies relative to the expected indices was evaluated for individual donors with the one-tailed z -test, and for all donors by means of analysis of variance (ANOVA) for mixed models, taking into account the repeated measures of treatments for each donor.…”

Section: Methodsmentioning

confidence: 99%

Adaptive response in human blood lymphocytes exposed to non-ionizing radiofrequency fields: resistance to ionizing radiation-induced damage

Sannino

Zeni

Romeo

et al. 2013

Journal of Radiation Research

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The aim of this preliminary investigation was to assess whether human peripheral blood lymphocytes which have been pre-exposed to non-ionizing radiofrequency fields exhibit an adaptive response (AR) by resisting the induction of genetic damage from subsequent exposure to ionizing radiation. Peripheral blood lymphocytes from four healthy donors were stimulated with phytohemagglutinin for 24 h and then exposed for 20 h to 1950 MHz radiofrequency fields (RF, adaptive dose, AD) at an average specific absorption rate of 0.3 W/kg. At 48 h, the cells were subjected to a challenge dose (CD) of 1.0 or 1.5 Gy X-irradiation (XR, challenge dose, CD). After a 72 h total culture period, cells were collected to examine the incidence of micronuclei (MN). There was a significant decrease in the number of MN in lymphocytes exposed to RF + XR (AD + CD) as compared with those subjected to XR alone (CD). These observations thus suggested a RF-induced AR and induction of resistance to subsequent damage from XR. There was variability between the donors in RF-induced AR. The data reported in our earlier investigations also indicated a similar induction of AR in human blood lymphocytes that had been pre-exposed to RF (AD) and subsequently treated with a chemical mutagen, mitomycin C (CD). Since XR and mitomycin-C induce different kinds of lesions in cellular DNA, further studies are required to understand the mechanism(s) involved in the RF-induced adaptive response.

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Section: Methodsmentioning

confidence: 99%

Adaptive response in human blood lymphocytes exposed to non-ionizing radiofrequency fields: resistance to ionizing radiation-induced damage

Sannino

Zeni

Romeo

et al. 2013

Journal of Radiation Research

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“…[ 26 ] was likely an outlier. It was well established that the development of RAR varied with individuals [ 69 ].…”

Section: Discussionmentioning

confidence: 99%

Non-induction of radioadaptive response in zebrafish embryos by neutrons

Kong

Kobayashi

et al. 2016

Journal of Radiation Research

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In vivo neutron-induced radioadaptive response (RAR) was studied using zebrafish (Danio rerio) embryos. The Neutron exposure Accelerator System for Biological Effect Experiments (NASBEE) facility at the National Institute of Radiological Sciences (NIRS), Japan, was employed to provide 2-MeV neutrons. Neutron doses of 0.6, 1, 25, 50 and 100 mGy were chosen as priming doses. An X-ray dose of 2 Gy was chosen as the challenging dose. Zebrafish embryos were dechorionated at 4 h post fertilization (hpf), irradiated with a chosen neutron dose at 5 hpf and the X-ray dose at 10 hpf. The responses of embryos were assessed at 25 hpf through the number of apoptotic signals. None of the neutron doses studied could induce RAR. Non-induction of RAR in embryos having received 0.6- and 1-mGy neutron doses was attributed to neutron-induced hormesis, which maintained the number of damaged cells at below the threshold for RAR induction. On the other hand, non-induction of RAR in embryos having received 25-, 50- and 100-mGy neutron doses was explained by gamma-ray hormesis, which mitigated neutron-induced damages through triggering high-fidelity DNA repair and removal of aberrant cells through apoptosis. Separate experimental results were obtained to verify that high-energy photons could disable RAR. Specifically, 5- or 10-mGy X-rays disabled the RAR induced by a priming dose of 0.88 mGy of alpha particles delivered to 5-hpf zebrafish embryos against a challenging dose of 2 Gy of X-rays delivered to the embryos at 10 hpf.

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Aberrant and multiaberrant (rogue) cells in peripheral lymphocytes of Hodgkin's lymphoma patients after chemotherapy

Ryabchenko¹,

Nasonova²,

Fesenko³

et al. 2006

Mutation Research/Fundamental and Molecular Mechanisms of Mutag

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Cytogenetic adaptive response in cultured human lymphocytes: dependence on the time of exposure to adapting and challenging doses of γ-rays

Cited by 20 publications

References 27 publications

Adaptive response in human blood lymphocytes exposed to non-ionizing radiofrequency fields: resistance to ionizing radiation-induced damage

Adaptive response in human blood lymphocytes exposed to non-ionizing radiofrequency fields: resistance to ionizing radiation-induced damage

Non-induction of radioadaptive response in zebrafish embryos by neutrons

Aberrant and multiaberrant (rogue) cells in peripheral lymphocytes of Hodgkin's lymphoma patients after chemotherapy

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