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Article ; Online: From radioresistance to radiosensitivity: In vitro evolution of L5178Y lymphoma.

Szumiel, Irena

International journal of radiation biology

2015 Volume 91, Issue 6, Page(s) 465–471

Abstract: Purpose: To discuss the possible reasons for the loss of tumourigenicity and the acquisition of new phenotypic features (among them, sensitivity to X and UVC radiations) as a result of in vitro cultivation of L5178Y lymphoma cells.: Results: Ten ... ...

Abstract	Purpose: To discuss the possible reasons for the loss of tumourigenicity and the acquisition of new phenotypic features (among them, sensitivity to X and UVC radiations) as a result of in vitro cultivation of L5178Y lymphoma cells. Results: Ten years ago the phenotypic differences between LY-R (original L5178Y maintained in vivo and examined in vitro) and LY-S lines were reviewed in detail by the author. The loss of tumourigenicity of LY-R cells upon in vitro cultivation accompanying the acquirement of the LY-S phenotype had been described earlier by Beer et al. (1983). In spite of their common origin, the sublines were shown to differ in their relative sensitivity to a number of DNA damaging agents and in numerous other features. Here, selected differences between LY-R and LY-S lines are briefly reviewed. It is proposed that Wallace's concept (2010a) that mitochondria are the interface between environmental conditions and the genome may explain the LY-R-LY-S conversion under prolonged in vitro cultivation. Conclusion: The differences between the LY lines were probably of epigenetic rather than genetic character. The properties of LY-R cells changed as a result of exposure to an oxic in vitro milieu. The changes could be preconditioned by heteroplasmy and the selection of cells endowed with mitochondria best fitted to a high oxygen-low carbon dioxide environment.
MeSH term(s)	Animals ; Biological Evolution ; Cell Line, Tumor ; Cell Proliferation ; DNA Damage ; Epigenesis, Genetic/radiation effects ; Genomic Instability/radiation effects ; Leukemia L5178/genetics ; Leukemia L5178/pathology ; Leukemia L5178/radiotherapy ; Mice ; Mitochondria/genetics ; Mitochondria/radiation effects ; Oxidative Stress/radiation effects ; Phenotype ; Radiation Tolerance/genetics ; Tumor Microenvironment/genetics ; Tumor Microenvironment/radiation effects
Language	English
Publishing date	2015-06
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	3065-x
ISSN	1362-3095 ; 0020-7616 ; 0955-3002
ISSN (online)	1362-3095
ISSN	0020-7616 ; 0955-3002
DOI	10.3109/09553002.2014.996263
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Article ; Online: Ionizing radiation-induced oxidative stress, epigenetic changes and genomic instability: the pivotal role of mitochondria.

Szumiel, Irena

International journal of radiation biology

2015 Volume 91, Issue 1, Page(s) 1–12

Abstract: Purpose: To review the data concerning the role of endogenously generated reactive oxygen species (ROS) in the non-targeted ionizing radiation (IR) effects and in determination of the cell population's fate, both early after exposure and after many ... ...

Abstract	Purpose: To review the data concerning the role of endogenously generated reactive oxygen species (ROS) in the non-targeted ionizing radiation (IR) effects and in determination of the cell population's fate, both early after exposure and after many generations. Conclusions: The short-term as well as chronic oxidative stress responses mainly are produced due to ROS generation by the electron transport chain (ETC) of the mitochondria and by the cytoplasmic NADPH oxidases. Whether the induction of the oxidative stress and its consequences occur or are hampered in a single cell largely depends on the interaction between the nucleus and the cellular population of several hundred or thousands of mitochondria that are genetically heterogeneous. High intra-mitochondrial ROS level is damaging the mitochondrial (mt) DNA and its mutations affect the epigenetic control mechanisms of the nuclear (n) DNA, by decreasing the activity of methyltransferases and thus, causing global DNA hypomethylation. These changes are transmitted to the progeny of the irradiated cells. The chronic oxidative stress is the main cause of the late post-radiation effects, including cancer, and this makes it an important adverse effect of exposure to IR and a target for radiological protection.
MeSH term(s)	Animals ; Carcinogenesis/radiation effects ; Epigenesis, Genetic/radiation effects ; Genomic Instability/radiation effects ; Humans ; Mitochondria/genetics ; Mitochondria/metabolism ; Mitochondria/radiation effects ; Oxidative Stress/radiation effects ; Reactive Oxygen Species/metabolism
Chemical Substances	Reactive Oxygen Species
Language	English
Publishing date	2015-01
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	3065-x
ISSN	1362-3095 ; 0020-7616 ; 0955-3002
ISSN (online)	1362-3095
ISSN	0020-7616 ; 0955-3002
DOI	10.3109/09553002.2014.934929
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Article ; Online: Intraclonal recovery of 'slow clones'-a manifestation of genomic instability: are mitochondria the key to an explanation?

Szumiel, Irena

Radiation and environmental biophysics

2014 Volume 53, Issue 3, Page(s) 479–484

Abstract: Intraclonal recovery following X-irradiation in an in vitro study of L5178Y-S murine leukaemic cells is reviewed. This phenomenon was first described in 1994 occurring in the slowly growing clones ('slow clones') present among the survivors in irradiated ...

Abstract	Intraclonal recovery following X-irradiation in an in vitro study of L5178Y-S murine leukaemic cells is reviewed. This phenomenon was first described in 1994 occurring in the slowly growing clones ('slow clones') present among the survivors in irradiated cell populations. An attempt to explain these experimental data is given in terms of the present knowledge of the role of mitochondria in nontargeted radiation effects, with the focus on genomic instability and mtDNA-related epigenetic modifications of the nuclear genome. An understanding of this intraclonal recovery may be important in preventing tumour regrowth following radiotherapy, as well as in decreasing the risk of secondary radiation-induced malignancies.
MeSH term(s)	Animals ; Cells, Cultured ; Clone Cells/cytology ; Clone Cells/metabolism ; Clone Cells/radiation effects ; Genomic Instability/radiation effects ; Humans ; Mitochondria/genetics ; Mitochondria/radiation effects ; X-Rays
Language	English
Publishing date	2014-03-18
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	124987-3
ISSN	1432-2099 ; 0301-634X
ISSN (online)	1432-2099
ISSN	0301-634X
DOI	10.1007/s00411-014-0532-y
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Article ; Online: Radiation hormesis: Autophagy and other cellular mechanisms.

Szumiel, Irena

International journal of radiation biology

2012 Volume 88, Issue 9, Page(s) 619–628

Abstract: Purpose: To review the cellular mechanisms of hormetic effects induced by low dose and low dose rate ionising radiation in model systems, and to call attention to the possible role of autophagy in some hormetic effects.: Results and conclusions: Very ...

Abstract	Purpose: To review the cellular mechanisms of hormetic effects induced by low dose and low dose rate ionising radiation in model systems, and to call attention to the possible role of autophagy in some hormetic effects. Results and conclusions: Very low radiation doses stimulate cell proliferation by changing the equilibrium between the phosphorylated and dephosphorylated forms of growth factor receptors. Radioadaptation is induced by various weak stress stimuli and depends on signalling events that ultimately decrease the molecular damage expression at the cellular level upon subsequent exposure to a moderate radiation dose. Ageing and cancer result from oxidative damage under oxidative stress conditions; nevertheless, ROS are also prominent inducers of autophagy, a cellular process that has been shown to be related both to ageing retardation and cancer prevention. A balance between the signalling functions and damaging effects of ROS seems to be the most important factor that decides the fate of the mammalian cell when under oxidative stress conditions, after exposure to ionising radiation. Not enough is yet known on the pre-requirements for maintaining such a balance. Given the present stage of investigation into radiation hormesis, the application of the conclusions from experiments on model systems to the radiation protection regulations would not be justified.
MeSH term(s)	Adaptation, Physiological ; Aging ; Animals ; Autophagy/physiology ; Cell Division/radiation effects ; DNA Damage ; Dose-Response Relationship, Radiation ; Hormesis ; Humans ; Neoplasms/prevention & control ; Oxidative Stress
Language	English
Publishing date	2012-09
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	3065-x
ISSN	1362-3095 ; 0020-7616 ; 0955-3002
ISSN (online)	1362-3095
ISSN	0020-7616 ; 0955-3002
DOI	10.3109/09553002.2012.699698
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Article ; Online: Autophagy, reactive oxygen species and the fate of mammalian cells.

Szumiel, Irena

Free radical research

2011 Volume 45, Issue 3, Page(s) 253–265

Abstract: The paper reviews the rapidly expanding pool of information on cellular and molecular mechanisms of autophagy, including autophagy types, macroautophagy induction, formation of autophagosomes and cross-talk between autophagy and apoptosis. Special ... ...

Abstract	The paper reviews the rapidly expanding pool of information on cellular and molecular mechanisms of autophagy, including autophagy types, macroautophagy induction, formation of autophagosomes and cross-talk between autophagy and apoptosis. Special attention is given to generation of reactive oxygen species (ROS) in various cellular compartments of cells under stress conditions inducing autophagy. The roles of hydrogen peroxide and superoxide in autophagy are analysed based on the recent experimental work. The relation between ROS and life span prolongation is briefly discussed, with the final conclusion that the paradox of dual role of ROS in life and death may be solved to a considerable extent due to research on autophagy.
MeSH term(s)	Aging ; Animals ; Apoptosis ; Autophagy ; Humans ; Hydrogen Peroxide/metabolism ; Phagosomes/metabolism ; Reactive Oxygen Species/metabolism ; Signal Transduction ; Stress, Physiological ; Superoxides/metabolism
Chemical Substances	Reactive Oxygen Species ; Superoxides (11062-77-4) ; Hydrogen Peroxide (BBX060AN9V)
Language	English
Publishing date	2011-03
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1194130-3
ISSN	1029-2470 ; 1071-5762
ISSN (online)	1029-2470
ISSN	1071-5762
DOI	10.3109/10715762.2010.525233
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Article: Epidermal growth factor receptor and DNA double strand break repair: the cell's self-defence.

Szumiel, Irena

Cellular signalling

2006 Volume 18, Issue 10, Page(s) 1537–1548

Abstract: The purpose of this review is to discuss the relation between the repair of DNA double strand breaks (DSB)--the main lethal lesion inflicted by ionising radiation-and the function of receptors of epidermal growth factor (EGFR) and similar ligands (other ... ...

Abstract	The purpose of this review is to discuss the relation between the repair of DNA double strand breaks (DSB)--the main lethal lesion inflicted by ionising radiation-and the function of receptors of epidermal growth factor (EGFR) and similar ligands (other members of the ERBB family). The reviewed experimental data support the assumption that in mammalian cells, one consequence of EGFR/ERBB activation by X-rays is its internalisation and nuclear translocation together with DNA-dependent protein kinase (DNA-PK) subunits present in lipid rafts or cytoplasm. The effect of EGFR/ERBB stimulation on DSB rejoining would be due to an increase in the nuclear content of DNA-PK subunits and hence, in activity increase of the DNA-PK dependent non-homologous end-joining (D-NHEJ) system. Such mechanism explains the radiosensitising action of "membrane-active drugs", hypertonic media, and other agents that affect nuclear translocation of proteins. Also, one radiosensitising effect of the recently introduced into clinical practice EGFR/ERBB inhibitors would consist on counteracting the nuclear translocation of DNA-PK subunits. In result, D-NHEJ may be less active in inhibitor-treated cells and this will contribute to an enhanced lethal effect of irradiation. The reviewed observations point to a heretofore not understood mechanism of the cell's self-defence against X-rays which can be exploited in combined radio- and chemotherapy.
MeSH term(s)	Animals ; Cell Nucleus/metabolism ; Cell Nucleus/radiation effects ; DNA Damage/genetics ; DNA Repair/genetics ; Humans ; Protein Transport/radiation effects ; Radiation Tolerance ; Receptor, Epidermal Growth Factor/metabolism
Chemical Substances	Receptor, Epidermal Growth Factor (EC 2.7.10.1)
Language	English
Publishing date	2006-10
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1002702-6
ISSN	0898-6568
ISSN	0898-6568
DOI	10.1016/j.cellsig.2006.03.010
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Zs.A 2579: Show issues

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Article ; Online: Chromatin acetylation, β-amyloid precursor protein and its binding partner FE65 in DNA double strand break repair.

Szumiel, Irena / Foray, Nicolas

Acta biochimica Polonica

2011 Volume 58, Issue 1, Page(s) 11–18

Abstract: Among post-translational modifications of chromatin proteins taking place in DNA double strand break (DSB) repair, acetylation plays a prominent role. This review lists several facts and hypotheses concerning this process. Lack of acetyltransferase TIP60 ...

Abstract	Among post-translational modifications of chromatin proteins taking place in DNA double strand break (DSB) repair, acetylation plays a prominent role. This review lists several facts and hypotheses concerning this process. Lack of acetyltransferase TIP60 (HIV-Tat interacting protein of 60 kDa) activity results in cells with defective DSB repair. The enzyme is present in the nucleus in a multimeric protein complex. TIP60 dependent activation of ATM (ataxia telangiectasia mutated kinase) is an early event in the response to DNA breakage. Other important acetylations are those of histones H4 and γH2AX. Correct reconstruction of the damaged site is critical for survival and prevention of genetic and epigenetic changes in the cell that may affect the function of its daughter cells. Recently, two proteins with previously unsuspected functions in DSB repair have been identified as active in this process: Alzheimer β-amyloid precursor protein (APP) and its binding partner FE65, β-amyloid precursor binding protein. Their participation in DSB repair in both neuronal and non-neuronal cells is related to acetylation carried out by the acetyltransferase complex. The same function is ascribed to heterochromatin protein 1 (HP1). So far, the relations (if any) between TIP60 activation by HP1 and by the FE65 complex remain unidentified.
MeSH term(s)	Acetylation ; Amyloid beta-Protein Precursor/genetics ; Amyloid beta-Protein Precursor/metabolism ; Animals ; Chromatin/metabolism ; DNA Breaks, Double-Stranded ; Histone Acetyltransferases/genetics ; Histone Acetyltransferases/metabolism ; Humans ; Nerve Tissue Proteins/genetics ; Nerve Tissue Proteins/metabolism ; Nuclear Proteins/genetics ; Nuclear Proteins/metabolism
Chemical Substances	APBB1 protein, human ; Amyloid beta-Protein Precursor ; Chromatin ; Nerve Tissue Proteins ; Nuclear Proteins ; Histone Acetyltransferases (EC 2.3.1.48)
Language	English
Publishing date	2011
Publishing country	Poland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	595762-x
ISSN	1734-154X ; 0001-527X
ISSN (online)	1734-154X
ISSN	0001-527X
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Article ; Online: Silver nanoparticles -- allies or adversaries?

Bartłomiejczyk, Teresa / Lankoff, Anna / Kruszewski, Marcin / Szumiel, Irena

Annals of agricultural and environmental medicine : AAEM

2013 Volume 20, Issue 1, Page(s) 48–54

Abstract: Nanoparticles (NP) are structures with at least one dimension of less than 100 nanometers (nm) and unique properties. Silver nanoparticles (AgNP), due to their bactericidal action, have found practical applications in medicine, cosmetics, textiles, ... ...

Abstract	Nanoparticles (NP) are structures with at least one dimension of less than 100 nanometers (nm) and unique properties. Silver nanoparticles (AgNP), due to their bactericidal action, have found practical applications in medicine, cosmetics, textiles, electronics, and other fields. Nevertheless, their less advantageous properties which make AgNP potentially harmful to public health or the environment should also be taken into consideration. These nanoparticles are cyto- and genotoxic and accumulate in the environment, where their antibacterial properties may be disadvantageous for agriculture and waste management. The presented study reviews data concerning the biological effects of AgNP in mammalian cells in vitro: cellular uptake and excretion, localization in cellular compartments, cytotoxicity and genotoxicity. The mechanism of nanoparticle action consists on induction of the oxidative stress resulting in a further ROS generation, DNA damage and activation of signaling leading to various, cell type-specific pathways to inflammation, apoptotic or necrotic death. In order to assure a safe application of AgNP, further detailed studies are needed on the mechanisms of the action of AgNP on mammalian cells at the molecular level.
MeSH term(s)	Animals ; Cells, Cultured ; Cytotoxins/chemistry ; Cytotoxins/toxicity ; Environmental Monitoring/methods ; Environmental Pollutants/chemistry ; Environmental Pollutants/toxicity ; Humans ; Metal Nanoparticles/chemistry ; Metal Nanoparticles/toxicity ; Mutagens/chemistry ; Mutagens/toxicity ; Silver/chemistry ; Silver/toxicity
Chemical Substances	Cytotoxins ; Environmental Pollutants ; Mutagens ; Silver (3M4G523W1G)
Language	English
Publishing date	2013
Publishing country	Poland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1215115-4
ISSN	1898-2263 ; 1232-1966
ISSN (online)	1898-2263
ISSN	1232-1966
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Zs.A 4242: Show issues

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Article ; Online: Signalling loops and linear pathways: NF-kappaB activation in response to genotoxic stress.

Brzóska, Kamil / Szumiel, Irena

Mutagenesis

2008 Volume 24, Issue 1, Page(s) 1–8

Abstract: The signalling loop concept was introduced in 1991 to explain activation of membrane and cytoplasmic kinases in response to DNA damage inflicted by ionizing radiation. Damage to the chromosomal DNA was thought to provide a primary signal and a secondary ... ...

Abstract	The signalling loop concept was introduced in 1991 to explain activation of membrane and cytoplasmic kinases in response to DNA damage inflicted by ionizing radiation. Damage to the chromosomal DNA was thought to provide a primary signal and a secondary signal from a nucleus to cytoplasm was assumed. This scenario was confirmed although not as originally proposed. A complex of nuclear factor-kappaB (NF-kappaB) essential modulator and ataxia telangiectasia-mutated kinase activated by genotoxic agents is sent to cytoplasm, prompting nuclear translocation of the active transcription factor NF-kappaB. In parallel, linear signalling pathways are initiated in the cytoplasm, mostly by reactive oxygen species, resulting in NF-kappaB activation and nuclear translocation. The choice of NF-kappaB activation pathway and the extent of activation of various pathways may be influenced by the relative degree of damage inflicted by genotoxic agents in the nuclear and cytoplasmic compartments. The ultimate pattern of cellular response is determined by availability, abundance and localization of the proteins participating in the signal transduction.
MeSH term(s)	Active Transport, Cell Nucleus ; Animals ; Ataxia Telangiectasia Mutated Proteins ; Carrier Proteins/metabolism ; Cell Cycle Proteins/metabolism ; Cell Nucleus ; DNA Breaks, Double-Stranded ; DNA Damage ; DNA-Binding Proteins/metabolism ; Death Domain Receptor Signaling Adaptor Proteins ; Humans ; Mice ; NF-kappa B/metabolism ; Protein-Serine-Threonine Kinases/metabolism ; Reactive Oxygen Species/metabolism ; Signal Transduction ; Tumor Suppressor Proteins/metabolism
Chemical Substances	Carrier Proteins ; Cell Cycle Proteins ; DNA-Binding Proteins ; Death Domain Receptor Signaling Adaptor Proteins ; NF-kappa B ; PIDD1 protein, human ; Reactive Oxygen Species ; Tumor Suppressor Proteins ; ATM protein, human (EC 2.7.11.1) ; Ataxia Telangiectasia Mutated Proteins (EC 2.7.11.1) ; Atm protein, mouse (EC 2.7.11.1) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2008-10-01
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	632903-2
ISSN	1464-3804 ; 0267-8357
ISSN (online)	1464-3804
ISSN	0267-8357
DOI	10.1093/mutage/gen056
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Article: Sirtuins (histone deacetylases III) in the cellular response to DNA damage--facts and hypotheses.

Kruszewski, Marcin / Szumiel, Irena

DNA repair

2005 Volume 4, Issue 11, Page(s) 1306–1313

Abstract: Histone deacetylases (HDAC) are an important member of a group of enzymes that modify chromatin conformation. Homologues of the yeast gene SIR2 in mammalian cells code type III histone deacetylases (HDAC III, sirtuins), dependent on NAD(+) and inhibited ... ...

Abstract	Histone deacetylases (HDAC) are an important member of a group of enzymes that modify chromatin conformation. Homologues of the yeast gene SIR2 in mammalian cells code type III histone deacetylases (HDAC III, sirtuins), dependent on NAD(+) and inhibited by nicotinamide. In yeast cells, Sir2 participates in repression of transcriptional activity and in DNA double strand break repair. It is assumed that certain sirtuins may play a similar role in mammalian cells, by modifying chromatin structure and thus, altering the accessibility of the damaged sites for repair enzymes. A relation between poly(ADP-ribosylation) and sirtuin function in cells with damaged DNA has been also postulated. Interconnections between NAD(+) metabolism, poly(ADP-ribosylation), DNA repair and gene expression should allow to modulate the cellular response to agents that damage DNA. Preliminary results, reviewed in this paper indicate that such possibility exists. We propose a hypothetical mechanism of sirtuin participation in DSB repair. It is based on the assumption that activation of PARP at the sites of DNA strand breaks leads to a local increase in nicotinamide concentration. Nicotinamide then inhibits sirtuins exactly at the site of DNA strand break. At present, however, there are no data directly confirming the effect of sirtuin inhibition on DSB repair processes in mammalian cells. Nevertheless, a connection between the acetylation status of histones and repair of DNA breaks has recently been found, indicating that all HDAC classes may modulate DNA repair processes. In addition, sirtuins exert an anti-apoptotic action in various cell types. Hence, it is possible to sensitise cells to apoptosis-inducing agents by sirtuin inhibitors.
MeSH term(s)	Animals ; DNA Damage/physiology ; DNA Repair/physiology ; Histone Deacetylases/genetics ; Histone Deacetylases/physiology ; Saccharomyces cerevisiae Proteins/genetics ; Saccharomyces cerevisiae Proteins/physiology ; Sirtuins/genetics ; Sirtuins/physiology
Chemical Substances	Saccharomyces cerevisiae Proteins ; Sirtuins (EC 3.5.1.-) ; Histone Deacetylases (EC 3.5.1.98) ; histone deacetylase 3 (EC 3.5.1.98)
Language	English
Publishing date	2005-11-21
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2071608-4
ISSN	1568-7856 ; 1568-7864
ISSN (online)	1568-7856
ISSN	1568-7864
DOI	10.1016/j.dnarep.2005.06.013
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