scholarly journals Corrigendum: Gamma Tocotrienol Protects Mice From Targeted Thoracic Radiation Injury

2021 ◽  
Vol 12 ◽  
Author(s):  
Vidya P. Kumar ◽  
Sasha Stone ◽  
Shukla Biswas ◽  
Neel Sharma ◽  
Sanchita P. Ghosh
2020 ◽  
Vol 11 ◽  
Author(s):  
Vidya P. Kumar ◽  
Sasha Stone ◽  
Shukla Biswas ◽  
Neel Sharma ◽  
Sanchita P. Ghosh

Radiation injury will result in multiorgan dysfuntion leading to multiorgan failure. In addition to many factors such as radiation dose, dose rate, the severity of the injury will also depend on organ systems which are exposed. Here, we report the protective property of gamma tocotrienol (GT3) in total as well as partial body irradiation (PBI) model in C3H/HeN male mice. We have carried out PBI by targeting thoracic region (lung-PBI) using Small Animal Radiation Research Platform, an X-ray irradiator with capabilities of an image guided irradiation with a variable collimator with minimized exposure to non-targeted tissues and organs. Precise and accurate irradiation of lungs was carried out at either 14 or 16 Gy at an approximate dose rate of 2.6 Gy/min. Though a low throughput model, it is amenable to change the field size on the spot. No damage to other non-targeted organs was observed in histopathological evaluation. There was no significant change in peripheral blood counts of irradiated mice in comparison to naïve mice. Femoral bone marrow cells had no damage in irradiated mice. As expected, damage to the targeted tissue was observed in the histopathological evaluation and non-targeted tissue was found normal. Regeneration and increase of cellularity and megakaryocytes on GT3 treatment was compared to significant loss of cellularity in saline group. Peak alveolitis was observed on day 14 post-PBI and protection from alveolitis by GT3 was noted. In irradiated lung tissue, thirty proteins were found to be differentially expressed but modulated by GT3 to reverse the effects of irradiation. We propose that possible mode of action of GT3 could be Angiopoietin 2-Tie2 pathway leading to AKT/ERK pathways resulting in disruption in cell survival/angiogenesis.


2007 ◽  
Vol 21 (5) ◽  
Author(s):  
James C Lee ◽  
Keith Cengel ◽  
Stathis Kanterakis ◽  
Ryan Krochak ◽  
Evguenia Arguiri ◽  
...  

2009 ◽  
Vol 8 (1) ◽  
pp. 47-53 ◽  
Author(s):  
James C Lee ◽  
Ryan Krochak ◽  
Aaron Blouin ◽  
Stathis Kanterakis ◽  
Shampa Chatterjee ◽  
...  

2000 ◽  
Vol 48 (3) ◽  
pp. 137-138
Author(s):  
M.T Munley ◽  
L.B Marks ◽  
P.H Hardenbergh ◽  
G.C Bentel ◽  
M.L Hernando ◽  
...  

2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
Shilpa Kulkarni ◽  
Kushal Chakraborty ◽  
K. Sree Kumar ◽  
Tzu-Cheg Kao ◽  
Martin Hauer-Jensen ◽  
...  

Purpose. This study was designed to determine the efficacy and mechanisms of radioprotection by the combination of gamma-tocotrienol (GT3) and pentoxifylline (PTX) against acute radiation injury. Materials and Methods. Post-irradiation survival was monitored to determine the most efficacious dose and time of administration of PTX. Dose reduction factor (DRF) was calculated to compare the radioprotective efficacy of the combination. To determine the mechanism of synergistic radioprotection by the combination, mevalonate or calmodulin were coadministered with the GT3-PTX combination. Mevalonate was used to reverse the inhibitory effect of GT3 on 3-hydroxy-3-methyl-glutaryl-CoA reductase (HMGCR), and calmodulin was used to reverse the inhibition of phosphodiesterase (PDE) by PTX. Results. The combination was most effective when 200 mg/kg of PTX was administered 15 min before irradiation along with 200 mg/kg of GT3 (−24 h) and resulted in a DRF of 1.5. White blood cells and neutrophil counts showed accelerated recovery in GT3-PTX-treated groups compared to GT3. Mevalonate had no effect on the radioprotection of GT3-PTX; calmodulin abrogated the synergistic radioprotection by GT3-PTX. Conclusion. The mechanism of radioprotection by GT3-PTX may involve PDE inhibition.


2001 ◽  
Vol 120 (5) ◽  
pp. A10-A10
Author(s):  
C HOUCHEN ◽  
B DIECKGRAEFE ◽  
M STUMOSKI ◽  
W STENSON

1967 ◽  
Vol 06 (02) ◽  
pp. 170-183
Author(s):  
K. Šilink ◽  
J. Němec ◽  
J. Kubal ◽  
S. Röhling ◽  
S. Vohnout

SummaryThe clinical course and the haematologic events in a patient suffering from metastatic thyroid cancer after administration of 806 mCi of 131I are described. A serious bone marrow depression developed and was treated successfully. The haematological changes during the early and late phases of the radiation injury were studied in detail and compared with those after external irradiation. The haematological events after internal irradiation with 131I are characterised by initial neutrophilic leukocytosis, protracted lymphopenia, slowly developing anaemia reaching lowest values about 3 months after administration, erythroid hyperplasia in the bone marrow after recovery from bone marrow depression and prominent cytological features of the bone marrow, especially pronounced erythropoietic polyploidy.


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