scholarly journals Adaptive Response in Zebrafish Embryos Induced Using Microbeam Protons as Priming Dose and X-ray Photons as Challenging Dose

2010 ◽  
Vol 51 (6) ◽  
pp. 657-664 ◽  
Author(s):  
Viann Wing Yan CHOI ◽  
Teruaki KONISHI ◽  
Masakazu OIKAWA ◽  
Hiroyuki ISO ◽  
Shuk Han CHENG ◽  
...  
2016 ◽  
Vol 57 (3) ◽  
pp. 210-219 ◽  
Author(s):  
Candy Y.P. Ng ◽  
Eva Y. Kong ◽  
Alisa Kobayashi ◽  
Noriyoshi Suya ◽  
Yukio Uchihori ◽  
...  

Abstract 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.


2018 ◽  
Author(s):  
Nitin Motilal Gandhi

AbstractPurposeCellular damage due to low dose of γ-radiation (≤0.1 Gy) is generally extrapolated from observing the effects at higher doses. These estimations are not accurate. This has led to uncertainties while assessing the radiation risk factors at low doses. Although there are reports on the radiation induced adaptive response, the mechanism of action is not fully elucidated, leading to the uncertainties. One of the outcomes of low dose radiation exposure is believed to be adaptive response. The mechanism of adaptive response is not fully understood. Therefore, the study was undertaken to understand the role of hypoxia inducible factor (HIF) on radiation induced adaptive response.Materials and methodsMCF-7 cells pre-exposed to low dose γ-radiation (0.1 Gy; Priming dose) were exposed to 2 Gy (challenging dose) 8 hrs after the priming dose and studied for the adaptive response. Cell death was measured by MTT assay, and apoptosis was measured by FACS analysis. DNA damage was measures by alkaline comet assay. HIF transcription activity was assayed using transiently transfected plasmid having HIF consensus sequence and luciferase as the reporter gene.ResultsCells when exposed to 0.1 Gy priming dose 8 hrs prior to the higher dose (2 Gy; Challenging dose) results in lower amount of radiation induced damages compared to the cells exposed to 2 Gy alone. Cobalt chloride treatment in place of priming dose also results in the protection to cells when exposed to challenging dose. There was up-regulation of HIF activity when cells were exposed to priming dose, indicating the role of HIF in radiation induced response.ConclusionResults indicate the γ-radiation induced adaptive response. One of the mechanism proposed is up-regulation of HIF after low dose exposure, which protects the cells from damages when they are exposed to challenging dose of 2 Gy radiation dose.


2017 ◽  
Vol 12 (7) ◽  
pp. 497-499
Author(s):  
Kalimuthu Kalishwaralal ◽  
Subhaschandrabose Jeyabharathi ◽  
Krishnan Sundar ◽  
Azhaguchamy Muthukumaran

2016 ◽  
Vol 161 (1) ◽  
pp. 24-27 ◽  
Author(s):  
S. I. Zaichkina ◽  
A. R. Dyukina ◽  
O. M. Rozanova ◽  
N. B. Simonova ◽  
S. P. Romanchenko ◽  
...  
Keyword(s):  

2016 ◽  
Vol 17 (8) ◽  
pp. 1321 ◽  
Author(s):  
E.Y. Kong ◽  
W.K. Yeung ◽  
T.K.Y. Chan ◽  
S.H. Cheng ◽  
K.N. Yu

2013 ◽  
Vol 33 (1) ◽  
pp. 91-100 ◽  
Author(s):  
V W Y Choi ◽  
Teruaki Konishi ◽  
Masakazu Oikawa ◽  
S H Cheng ◽  
K N Yu

Zygote ◽  
1997 ◽  
Vol 5 (2) ◽  
pp. 153-175 ◽  
Author(s):  
Richard Ikegami ◽  
Alma K. Rivera-Bennetts ◽  
Deborah L. Brooker ◽  
Thomas D. Yager

SummaryWe address the developmental activation, in the zebrafish embryo, of intrinsic cell-cycle checkpoints which monitor the DNA replication process and progression through the cell cycle. Eukaryotic DNA replication is probably carried out by a multiprotein complex containing numerous enzymes and accessory factors that act in concert to effect processive DNA synthesis (Applegren, N. et al. (1995) J. Cell. Biochem. 59, 91–107). We have exposed early zebrafish embryos to three chemical agents which are predicted to specifically inhibit the DNA polymerase α, topoisomerase I and topoisomerase II components of the DNA replication complex. We present four findings: (1) Before mid-blastula transition (MBT) an inhibition of DNA synthesis does not block cells from attempting to proceed through mitosis, implying the lack of functional checkpoints. (2) After MBT, the embryo displays two distinct modes of intrinsic checkpoint operation. One mode is a rapid and complete stop of cell division, and the other is an ‘adaptive’ response in which the cell cycle continues to operate, perhaps in a ‘repair’ mode, to generate daughter nuclei with few visible defects. (3) The embryo does not display a maximal capability for the ‘adaptive’ response until several hours after MBT, which is consistent with a slow rranscriptional control mechanism for checkpoint activation. (4) The slow activation of checkpoints at MBT provides a window of time during which inhibitors of DNA synthesis will induce cytogenetic lesions without killing the embryo. This could be useful in the design of a deletion-mutagenesis strategy.


2018 ◽  
Vol 24 (S2) ◽  
pp. 406-407
Author(s):  
G. Schulz ◽  
E. Corek ◽  
S. Siegrist ◽  
P. Thalmann ◽  
H. Deyhle ◽  
...  

2013 ◽  
Vol 33 (1) ◽  
pp. 101-112 ◽  
Author(s):  
V W Y Choi ◽  
C Y P Ng ◽  
M K Y Kong ◽  
S H Cheng ◽  
K N Yu

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