LIFE01200604005 Shri Somnath Ghosh - Homi Bhabha National ...

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CHAPTER 3 RESULTS in all the cells. The average numbers of foci after 15min of 2Gy gamma irradiation were 24±5, while after 2Gy oxygen irradiation; the foci were 28±4.7 (Fig. 3.3.2.2 A & C). Thus unlike the cell survival, the difference in induction of γ-H2AX foci 15 min after 2Gy of either radiation was not as profound. Activation of signaling molecules at dose of 2Gy of gamma radiation was studied because the initial response manifested as double strand breaks, as indicated by γ-H2AX foci, was found to be almost the same at 2Gy of either radiation. Since the RBE of oxygen ions was nearly 3, it would be more logical to compare 2Gy of oxygen ion with 6Gy of gamma ray. The average numbers of foci after 15min of 6Gy gamma irradiation were 35±3.5 (Fig. 3.3.2.2 A & C). Thus, 6Gy gamma ray induced 1.25 times more foci than 2Gy oxygen ions. The γ-H2AX foci were also counted 4 hours after irradiation to compare the repair status at that time. 53% of 2Gy gamma irradiated cells still showed γ-H2AX foci but the average foci per cell had reduced to only 4.3±2.2, where as 100% of 6Gy gamma irradiated cells showed γ-H2AX foci and the average foci per cell had reduced to only 8±2.5. In oxygen ion irradiated cells, although bright green γ-H2AX intensity was observed till 4 hours in 60% of cells, there was a significant reduction in appearance of distinct foci like structures (10±2) (Fig. 3.3.2.2 B & C). Disappearance of γ-H2AX foci indicates DNA repair/rejoining. However, from the survival data of A549 cells it was clear that in oxygen irradiated cells the repair of DNA had not taken place. The result was so intriguing that it was essential to measure the total intensity of γ-H2AX in irradiated cells. Instead of counting number of foci, the intensity of γ-H2AX in cells showing the foci was estimated by ImageJ software in the same images. In case of 2Gy or 6Gy gamma irradiation, both γ-H2AX foci and its total intensity levels had reduced at 4 hours (Fig. 3.3.2.2 D). However, in case of oxygen irradiation, the total intensity of γ-H2AX at 4 hours was yet very high (Fig. 3.3.2.2D) although foci were not properly visible. This could indicate diffusion of γ- 159
CHAPTER 3 RESULTS H2AX foci rather than its disappearance due to actual dephosphorylation of γ-H2AX. Presence of γ-H2AX even 4 hours after oxygen ion irradiation suggests that DNA had not been repaired. Fig. 3.3.2.2 Phosphorylation of H2AX (γ-H2AX) at different time points after exposure to 2Gy and 6Gy gamma or 2Gy oxygen irradiation in A549 cells. Representative image showing γ- H2AX foci (A) 15 minutes and (B) 4 hours after irradiation. Each phospho-H2AX antibody was indirectly labeled with Molecular Probe 488 secondary antibody (green) and cells were mounted with ProLong Gold antifede with DAPI (blue). All images were captured using Carl Zeiss confocal microscope with the same exposure time. (C) Graph represents average numbers of foci per cell, percentage of cells showing the foci is marked above the bars. (D) Graph represents relative intensity of γ-H2AX as determined by ImageJ software. At least 100 cells per experiment were analyzed from three independent experiments. Data represents means ± SD of three independent experiments; significantly different from unirradiated controls: *P < 0.05, **P < 0.01. 160
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RADIATION INDUCED SIGNALING IN MAMM
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DECLARATION I, hereby declare that
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CONTENTS Page No. SYNOPSIS………
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2.11 Measurement of NO production
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PREAMBLE SYNOPSIS Ionising radiatio
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SYNOPSIS Aims and Objectives: To St
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SYNOPSIS 2.6 Immunofluorescence sta
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SYNOPSIS ATM gene expression, which
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SYNOPSIS Percentage Survival 100 80
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SYNOPSIS Ratio of Rad52 to Actin Ra
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Relative Phosphorylation 45 40 35 3
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SYNOPSIS Fig. 3.3A Clonogenic Cell
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SYNOPSIS (A) Av No. of phospho BRCA
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SYNOPSIS Percentage Survival 120 10
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SYNOPSIS Fig.3.4B. Existance of cro
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SYNOPSIS Fig. 3.4EDNA damage in EL-
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SYNOPSIS subsequent cytotoxicity ca
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SYNOPSIS [4] Hall, E. J. Radiobiolo
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CHAPTER 1 INTRODUCTION INTRODUCTION
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CHAPTER 1 INTRODUCTION 15.8% 9.56%
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CHAPTER 1 INTRODUCTION far apart an
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CHAPTER 1 INTRODUCTION and are more
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CHAPTER 1 INTRODUCTION 1.3 DNA dama
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CHAPTER 1 INTRODUCTION associates w
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CHAPTER 1 INTRODUCTION are unable t
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CHAPTER 1 INTRODUCTION Perhaps one
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CHAPTER 1 INTRODUCTION occurs at DS
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CHAPTER 1 INTRODUCTION related prot
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CHAPTER 1 INTRODUCTION damage must
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CHAPTER 1 INTRODUCTION At the prese
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CHAPTER 1 INTRODUCTION predominant
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CHAPTER 1 INTRODUCTION provide a me
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CHAPTER 1 INTRODUCTION hypersensiti
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CHAPTER 1 INTRODUCTION cycle-specif
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CHAPTER 1 INTRODUCTION 1.4 Overview
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CHAPTER 1 INTRODUCTION 1.4.1 Radiat
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CHAPTER 1 INTRODUCTION interaction
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CHAPTER 1 INTRODUCTION p90S6 kinase
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CHAPTER 1 INTRODUCTION CD4 (formerl
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CHAPTER 1 INTRODUCTION unrepaired d
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CHAPTER 1 INTRODUCTION well to the
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CHAPTER 1 INTRODUCTION 1.6 Radiatio
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CHAPTER 1 INTRODUCTION becomes pote
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CHAPTER 2 MATERIALS AND METHODS MAT
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CHAPTER 2 MATERIALS AND METHODS 2.2
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CHAPTER 2 MATERIALS AND METHODS res
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CHAPTER 2 MATERIALS AND METHODS Arr
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CHAPTER 2 MATERIALS AND METHODS PBS
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CHAPTER 2 MATERIALS AND METHODS the
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CHAPTER 2 MATERIALS AND METHODS 2.1
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CHAPTER 3 RESULTS RESULTS 93
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CHAPTER 3 RESULTS fractionated regi
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CHAPTER 3 RESULTS On comparison of
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CHAPTER 3 RESULTS Table 3.1.2A List
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CHAPTER 3 RESULTS 80 NM_002185 IL7R
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CHAPTER 3 RESULTS SAA2 149 AU134977
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CHAPTER 3 RESULTS 221 LOC643167 RNA
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CHAPTER 3 RESULTS 299 BF244402 FBXO
Page 118 and 119: CHAPTER 3 RESULTS CDK4) 57 AU152107
Page 120 and 121: CHAPTER 3 RESULTS 134 AL045793 METT
Page 122 and 123: CHAPTER 3 RESULTS 58 AF237813 ABAT
Page 124 and 125: CHAPTER 3 RESULTS 127 AI809749 ORMD
Page 126 and 127: CHAPTER 3 RESULTS 31 BE615699 UNC84
Page 128 and 129: CHAPTER 3 RESULTS 47 AF026303 SULT1
Page 130 and 131: CHAPTER 3 RESULTS 117 BF062193 CYor
Page 132 and 133: CHAPTER 3 RESULTS 187 AL036662 ---
Page 134 and 135: CHAPTER 3 RESULTS 52 AV686514 EMP2
Page 136 and 137: CHAPTER 3 RESULTS exposed to 10 Gy
Page 138 and 139: CHAPTER 3 RESULTS Fig.3.1.4 Gene ex
Page 140 and 141: CHAPTER 3 RESULTS Fig. 3.1.6 Radiat
Page 142 and 143: CHAPTER 3 RESULTS Fig. 3.1.7 Transl
Page 144 and 145: CHAPTER 3 RESULTS 3.1.9 Stabilizati
Page 146 and 147: CHAPTER 3 RESULTS 23±1.5% (Fig. 3.
Page 148 and 149: CHAPTER 3 RESULTS whereas only the
Page 154 and 155: CHAPTER 3 RESULTS with equal doses
Page 156 and 157: CHAPTER 3 RESULTS Fig.3.3.1.2 Forma
Page 158 and 159: CHAPTER 3 RESULTS Fig.3.3.1.3 Phosp
Page 160 and 161: CHAPTER 3 RESULTS (7.5±0.64) (Fig.
Page 164 and 165: CHAPTER 3 RESULTS Fig.3.3.1.7b Phos
Page 166 and 167: CHAPTER 3 RESULTS 3.3.2 Oxygen beam
Page 170 and 171: CHAPTER 3 RESULTS 3.3.2.3 Radiation
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Page 178 and 179: CHAPTER 3 RESULTS PMA stimulated U9
Page 180 and 181: CHAPTER 3 RESULTS Fig.3.4.2. Exista
Page 182 and 183: CHAPTER 3 RESULTS up-regulation of
Page 184 and 185: CHAPTER 3 RESULTS Fig.3.4.3.2 NO pr
Page 186 and 187: CHAPTER 3 RESULTS 3.4.3.4 Apoptotic
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Page 190 and 191: CHAPTER 3 RESULTS Fig.3.4.4b DNA da
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CHAPTER 4 DISCUSSION inhibition of
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CHAPTER 4 DISCUSSION The survival o
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CHAPTER 5 REFERENCES [1] Khan, F. T
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CHAPTER 5 REFERENCES [19] Woo, R. A
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CHAPTER 5 REFERENCES [35] Nghiem, P
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CHAPTER 5 REFERENCES [52] McKay, B.
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CHAPTER 5 REFERENCES [69] Cary, R.
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CHAPTER 5 REFERENCES [84] Uziel, T.
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CHAPTER 5 REFERENCES [98] Liu, Y.;
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CHAPTER 5 REFERENCES [111] Fei, P.;
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CHAPTER 5 REFERENCES [127] Frank, K
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CHAPTER 5 REFERENCES [141] Pierce,
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CHAPTER 5 REFERENCES [156] Roots, R
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CHAPTER 5 REFERENCES [171] Xia, Z.;
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CHAPTER 5 REFERENCES (MAP) kinase c
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CHAPTER 5 REFERENCES phosphorylatio
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CHAPTER 5 REFERENCES [211] Anderson
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CHAPTER 5 REFERENCES [229] Konca, K
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CHAPTER 5 REFERENCES [245] Kastan,
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CHAPTER 5 REFERENCES [261] Miralbel
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CHAPTER 5 REFERENCES [278] Weizman,
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CHAPTER 5 REFERENCES [294] Zhou, H.
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PUBLICATIONS AND PRESENTATIONS Publ
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Mutation Research 729 (2012) 61-72
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S. Ghosh, M. Krishna / Mutation Res
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Cancer Invest Downloaded from infor
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1568 I. J. Radiation Oncology d Bio
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