Early Postirradiation Chromatin Degradation in Thymocytes

Soldatenkov, Viatcheslav A.; Denisenko, M.F.; Khodarev, Nikolai N.; Votrin, I. I.; Filippovich, I V

doi:10.1080/09553008914550981

Cited by 13 publications

(8 citation statements)

References 16 publications

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“…after irradiation or injection). 4,5,28 The time-course of thymocyte DNA fragmentation by 5-Gy whole-body irradiation showed that the degradation was detectable as early as 3 hr after irradiation (Fig. 4b).…”

Section: In Vivo Degradation Of Thymocyte Dna During Thymic Atrophymentioning

confidence: 99%

“…21 Egg PC, at a ®nal concentration of 480 mM with 0Á1 mCi 1,2-di [1][2][3][4][5][6][7][8][9][10][11][12][13][14] C]palmitoyl PC, was dried under N 2 stream in the presence of 5 mM oleate and 1 mM PA. To this lipid mixture, an aqueous solution containing 10 mM CaCl 2 , 25 mM KF, 1Á5% (vol/vol) ethanol, and 50 mM HEPES, pH 7Á0, was added and sonicated in a bathtype sonicator for 1 min at room temperature. After addition of 20 ml of crude membrane suspension, the reaction mixture was incubated for 90 min at 308.…”

Section: Enzyme Sourcesmentioning

confidence: 99%

“…The thymocyte death follows a typical pattern of apoptosis identi®ed by fragmentation of DNA as a result of endonuclease activation. 4,5 Apoptotic cells are eventually phagocytosed by macrophages and neighbouring cells in vivo. 6 In fact, macrophages phagocytosing apoptotic thymocytes in situ are found in thymus during radiation-induced apoptosis.…”

Section: Introductionmentioning

confidence: 99%

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Elevation of oleate‐activated phospholipase D activity during thymic atrophy

et al. 2002

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SUMMARYVarious phospholipases are thought to be associated with the in vitro apoptosis of thymocytes. In the present study, the in vivo phospholipase D (PLD) activity of rat thymus was studied after wholebody X-irradiation or injection of dexamethasone (DEX). Using exogenous [14 C]dipalmitoyl phosphatidylcholine (PC) as the substrate, an elevation of oleate-activated PLD activity was observed during thymic atrophy. The activity increases were sevenfold at 48 hr after 5-Gy irradiation and fourfold at 72 hr after injection of 5 mg/kg DEX. The elevation of PLD activity appeared to parallel extensive thymus shrinkage. An increased level of thymic phosphatidic acid (PA), the presumed physiological product of PLD action on PC, was also detected. By comparing the acyl chains of PA with those of other phospholipids, PA appeared to originate from PC. To assess the role of PLD during thymic atrophy, thymocytes and stromal cells were isolated. Although thymocytes themselves exhibited signi®cant PLD activation, the major elevation in PLD activity (greater than fourfold) was found in isolated stromal cells. PLD was also activated during in vitro phagocytosis of apoptotic thymocytes by the macrophage-like cell line P388D1. This in vitro phagocytosis was signi®cantly inhibited by PLD action blockers, such as 2,3-diphosphoglycerate and 1-butanol. These observations strongly suggest that the alteration of oleate-activated PLD activity is part of an in vivo event in the progression of thymic atrophy, including phagocytic clearance of apoptotic thymocytes.

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Section: In Vivo Degradation Of Thymocyte Dna During Thymic Atrophymentioning

confidence: 99%

Section: Enzyme Sourcesmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Elevation of oleate‐activated phospholipase D activity during thymic atrophy

et al. 2002

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“…In contrast to mitotic cell death, apoptosis is a relatively rapid and irreversible process which occurs within a few hours following IR exposure. Although documented in proliferating cell lines as well as tumor cells (Bump et al, 1994), IR-induced apoptosis was originally described in nonmitotic cells such as lymphocytes, which lead to the term of interphase cell death (Yamada and Ohyama, 1988;Soldatenkov et al, 1989).…”

Section: Introductionmentioning

confidence: 99%

Lack of ceramide generation in TF-1 human myeloid leukemic cells resistant to ionizing radiation

et al. 1998

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The mechanism(s) by which ionizing radiation (IR) induces cell death is of fundamental importance in understanding cell sensitivity and resistance. Here we evaluated the response to IR of two subclones of the autonomous human erythromyeloblastic cell line TF-1: TF-1-34 (which expresses CD34) and TF-1-33 (which lacks CD34). In clonogenic assays, TF-1-34 cells were found to be relatively less sensitive to IR compared to TF-1-33 cells based on the D 0 determination (3.01 vs 1.56 Gy). Furthermore, after IR at 12 Gy, TF-1-33 cell viability decreased by *50% within 24 h, whereas TF-1-34 cell growth was unaffected during this time. Gradual loss of TF-1-34 cell viability was observed only after 48 h. Morphological and molecular analysis revealed that TF-1-33 cells died of apoptosis, and TF-1-34 cells of delayed reproductive cell death. While IR produced comparable amounts of DNA double strand breaks (DSB) in both cell lines, TF-1-34 retained DSB much longer than TF-1-33 suggesting that radioresistance and the defective apoptotic response of TF-1-34 cells was not related to a higher DNA repair capacity. However, the lack of an apoptotic response in TF-1-34 was correlated to the absence of a sphingomyelin (SM)-ceramide (CER) signaling pathway. Indeed, IR triggered in TF-1-33 cells but not in TF-1-34, SM hydrolysis (25% at 12 Gy) and CER generation (450%) through the activation of neutral but not acid sphingomyelinase. Synthetic cell permeate CER induced apoptosis in both TF-1-33 and TF-1-34 cells. This study indicates that alterations of the SM-CER signaling pathway can significantly influence the cell death process as well as the survival of acute myeloid leukemia cells after IR exposure.

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“…As shown in Figure 1, the presumed chain of events leads to Ca t + ion influx, activation of endonuclease, and DNA fragmentation as the immediate cause of cell death . Essentially the same features characterize radiation-induced apoptosis of thymocytes : DNA degradation (Soldatenkov et al 1989) and dependence on Cat + ions (Story et al 1992) . The apoptotic cells can be rescued by treatment with aurintricarboxylic acid (ATA), an inhibitor of endonuclease, although the specificity of ATA is doubtful (Eastman 1993) ; the sparing effect is reflected in both viability increase and decreased DNA fragmentation .…”

Section: Dna Damage and Degradationmentioning

confidence: 97%

Ionizing Radiation-induced Cell Death

Szumiel

1994

International Journal of Radiation Biology

108

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Selected aspects of radiation-induced cell death, connected with signal transduction pathways are reviewed. Cell death is defined as insufficiency of the cellular signal transducing system to maintain the cell's physiological functions. The insufficiency may be due to impaired signal reception and/or transduction, lack or erroneous transcription activation, and eventual cellular 'misexpression' of the signal. The molecular basis of this insufficiency would be damage to genomic (but also other cellular) structures and closing of specific signalling pathways or opening of others (like those leading to apoptosis). I describe experimental data that suggest an important role of RAS/NF1 and p53/p105 Rb proteins in cell cycle control-coupled responses to DNA damage.

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Early Postirradiation Chromatin Degradation in Thymocytes

Cited by 13 publications

References 16 publications

Elevation of oleate‐activated phospholipase D activity during thymic atrophy

Elevation of oleate‐activated phospholipase D activity during thymic atrophy

Lack of ceramide generation in TF-1 human myeloid leukemic cells resistant to ionizing radiation

Ionizing Radiation-induced Cell Death

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