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1
Content available The rapid interphase chromosome assay (RICA) implementation : comparison with other PCC methods
Sommer S., Buraczewska I., Sikorska K., Bartłomiejczyk T., Szumiel I., Kruszewski M.
Nukleonika
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2015
|
Vol. 60, No. 4, part 2
933--941
EN
A report is presented on the advantages of the rapid interphase chromosome assay (RICA) and the difficulties that may be met while implementing this method for application in biological dosimetry. The RICA test can be applied on unstimulated human lymphocytes; this is an advantage in comparison with the dicentric chromosomes or micronucleus tests. In the former two tests, stimulated lymphocytes are examined and hence, 48 h more are needed to obtain cells traversing the cell cycle. Due to the use of unstimulated nondividing cells, higher numbers of cells are available for RICA analysis than for dicentric chromosomes or micronuclei tests. Moreover, the method can be applied after exposure to ionizing radiation doses in excess of 5 Gy. Such doses cause a signifi cant cell cycle delay or result in the loss of G2 phase and mitotic cells because of apoptosis. Therefore, the traditional biodosimetry based on the evaluation of the incidence of damage to chromosomes is very difficult to carry out. This is due to the lack of an adequate number of mitotic cells for analysis. RICA is free of this disadvantage. An automatic microscope can be used to retrieve cell images; automatic image analysis can also be used.
2
Content available Wolno rosnące klony komórek białaczki L5178Y i zagadka wewnątrzklonalnej odnowy popromiennej
Szumiel I.
Postępy Techniki Jądrowej
|
2014
|
z. 1
37--40
3
Content available Hormeza popromienna: autofagia i inne mechanizmy komórkowe
Szumiel I.
Postępy Techniki Jądrowej
|
2012
|
z. 1
7--15
4
Content available Treatment with silver nanoparticles delays repair of X-ray induced DNA damage in HepG2 cells
Wojewódzka M., Lankoff A., Dusińska M., Brunborg G., Czerwińska J., Iwaneńko T., Stępkowski T., Szumiel I., Kruszewski M.
Nukleonika
|
2011
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Vol. 56, No. 1
29-33
EN
Nanoparticles (NPs) defined as particles having at least one dimension below 100 nm have been applied in the last decade in industry and medicine. Recently, there is an increased concern about the biohazard aspect of the presence of NP in consumer goods and in the environment. Silver NP (Ag NP) cause oxidative stress in mammalian cells in result of generation of reactive oxygen species (ROS). This results in genotoxicity and mutagenicity, disturbed mitochondrial respiration, slowed proliferation and cell death. Using the alkaline comet assay, we examined the effect of combined treatment with Ag NP 20 nm or 200 nm and X-rays (2 Gy) in HepG2 cells. In addition, combined treatment with X-rays and titanium dioxide NP (TiO2 NP) 21 nm was also studied. No effect of NP pre-treatment on X-ray induced initial deoxyribonucleic acid (DNA) damage levels was observed for all three NP. In contrast, Ag NP treatment preceding exposure to X-rays caused a marked decrease in the rate of single strand break rejoining. The effect was particularly strong for Ag NP 20 nm. TiO2 NP pre-treatment had no effect on DNA repair.
5
Content available remote PCC w biodozymetrii - mechanizm molekularny, zalety i wady
Sommer S., Szumiel I.
Postępy Techniki Jądrowej
|
2010
|
z. 3
35-38
6
Content available remote Radiobiologia w służbie medycyny
Grądzka I., Szumiel I.
Postępy Techniki Jądrowej
|
2009
|
z. 1
7-11
7
Content available remote PCC w biodozymetrii - mechanizm biomolekularny zalety i wady
Sommer S., Szumiel I.
Postępy Techniki Jądrowej
|
2009
|
z. 4
34-37
8
Content available remote Dozymeria biologiczna w służbie energetyki jądrowej
Kruszewski M., Sommer S., Szumiel I.
Postępy Techniki Jądrowej
|
2009
|
z. 3
21-26
9
Content available Charge transfer in DNA and repair of oxidative damage
Męczyńska S., Szumiel I.
Nukleonika
|
2009
|
Vol. 54, No. 1
11-16
EN
The possibility of a biological role of an unusual function of DNA sequences is discussed, namely, signaling by charge transfer within chromatin. Although a general conclusion on its biological significance is premature, the idea of charge transfer accompanying repair of some types of oxidative DNA damage is based on sound experimental data. Both physical and chemical experiments reviewed here provided results indicating that DNA duplex under certain conditions (among them – hydration) – can behave as narrow band gap semiconductor. With the use of model molecules it was shown that charge transfer most probably occurs by hopping between guanine residues and tunneling through thymine-adenine (TA) base pairs. Charge transfer is nucleotide sequence and distance dependent. Furthermore, the pi-stacked base pairs must be perfectly matched to mediate charge transfer and in a damaged double helix this condition is not fulfilled. Hence, the possibility that charge transfer takes place in oxidatively damaged DNA after UV or X-irradiation and it becomes interrupted by mismatched base pairs, thus signaling the mismatch or strand break to the repair machinery. Function of base damage repair enzymes which contain [4Fe-4S] clusters is discussed in this context.
10
Content available remote Sprzężone dieny kwasu linolowego [CLA] hamują naprawę DNA uszkodzonego przez promieniowanie X
Grądzka I., Szumiel I.
Postępy Techniki Jądrowej
|
2008
|
z. 3
24-28
11
Content available Relationships between EGFR-initiated signalling, DNA double-strand break rejoining and survival in X-irradiated human glioma M059 cells
Grądzka I., Buraczewska I., Szumiel I.
Nukleonika
|
2008
|
Vol. 53, No. 2
37-44
EN
The aim of this study was to investigate the effect of signalling inhibition on survival and double-strand break (DSB) rejoining in cells differing in sensitivity to inhibitors, X-rays and bleomycin. Human glioma M059 cells, K (relatively radioresistant) and J (radiosensitive, defective in DSB rejoining for lack of DNA-dependent protein kinase catalytic subunit, DNA-PKcs) were pretreated with signalling inhibitors: tyrphostin AG 1478, specific for epidermalgrowth- factor-receptor (EGFR) kinase or PD 98059, specific for kinase MEK 1/2 (mitogen-activated, extracellular signal-activated kinases 1 and 2). Subsequently, the cells were X-irradiated or treated with bleomycin. Cell survival was determined by clonogenicity test. DSB rejoining was monitored with the use of pulsed-field gel electrophoresis (PFGE). We found that in X-irradiated M059 K cells EGFR kinase activity was necessary for efficient DSB rejoining and the kinase inhibitor, tyrphostin AG 1478, acted as radiosensitizer in the dose range that reduced cell survival to 0.7-0.8. Inhibition of EGFR kinase, however, did not decrease survival or affect DSB rejoining in DNA-PKcs-deficient M059 J cells. These results indicated that the decrease in cell survival was due to a disturbed DSB rejoining by the DNA-PK dependent system. In contrast, inhibition of MEK 1/2 kinase on EGFR downstream signalling pathway by PD 98059 did not affect DSB rejoining in either cell line and exerted a radioprotective effect.
12
Content available remote Samoobrona komórkowa receptor czynnika wzrostowego pobudza naprawę DNA uszkodzonego przez promieniowanie X
Grądzka I., Sochanowicz B., Szumiel I.
Postępy Techniki Jądrowej
|
2007
|
z. 2
2-8
13
Content available remote Dlaczego komórki różnią się promieniowrażliwością?
Szumiel I.
Postępy Techniki Jądrowej
|
2007
|
z. 4
18-24
14
Content available remote Ogniska histonu [gamma]-H2AX marker pęknięć podwójnoniciowych DNA
Wojewódzka M., Szumiel I.
Postępy Techniki Jądrowej
|
2006
|
z. 3
15-18
15
Content available remote Indywidualna promieniowrażliwość chromosomów i odcisk palca promieniowania. Otwarte pytania w dziedzinie dozymetrii biologicznej
Sommer S., Deperas-Kamińska M., Wójcik A., Szumiel I.
Postępy Techniki Jądrowej
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2006
|
z. 1
16-21
16
Content available remote Hormeza czy to zjawisko powszechne i powszechnie nieznane?
Wójcik A., Szumiel I., Liniecki J.
Postępy Techniki Jądrowej
|
2006
|
z. 2
34-39
PL
Czy promieniowanie jonizujące w zakresie niskich dawek promieniowania szkodzi zdrowiu, czy mu służy? To pytanie pozostaje przedmiotem gorących dyskusji. Chcemy pokazać, dlaczego trudno jest uzyskać na nie decydującą odpowiedź oraz przedstawić zasady, na jakich w takiej sytuacji powinny się opierać normy ochrony radiologicznej.
17
Content available Effects of an antimutagen of 1,4-dihydropyridine series on cell survival and DNA damage in L5178Y murine sublines
Dalivelya O., Savina N., Kuzhir T., Buraczewska I., Wojewódzka M., Szumiel I.
Nukleonika
|
2006
|
Vol. 51, nr 3
141-146
EN
In a series of studies it was shown that 1,4-dihydropyridine derivatives (1,4-DHP) show antimutagenic and anticlastogenic properties and accelerate repair of oxidant and ionising radiation generated DNA damage. Here, effects of one of 1,4-DHP compounds (sodium 3,5-bis-ethoxycarbonyl-2,6-dimethyl-1,4-dihydropyridine-4-carboxylate denoted as DHP) in X-irradiated L5178Y cells (murine lymphoma sublines, LY-R and LY-S) are reported. DHP treatment 1 h before, during and after X-irradiation gave a radioprotective effect in double strand break (DSB) repair competent LY-R cells: there was an increase in post-irradiation proliferation and cell viability as well as a slight acceleration of break rejoining as measured by the neutral comet assay. In the radiosensitive LY-S cells with impaired non-homologous end-joining system, the radioprotective effect was seen as enhanced growth and viability. There was, however, no effect on the DSB repair rate. Notably, there was no dependence of the biological effects on DHP concentration in the range of concentrations studied (1 nM - 100 mM), suggesting an all-or-none effect, as in cellular signaling induction observed in radioadaptation or bystander effect. We assume that DHP acts by decreasing fixation of radiation inflicted DNA damage, among others, by increasing the rate of DNA repair and enhancing the efficiency of checkpoint control. Direct confirmation of this assumption is necessary.
18
Content available DNA double-strand break rejoining in radioadapted human lymphocytes: evaluation by neutral comet assay and pulse-field gel electrophoresis
Wojewódzka M., Buraczewska I., Szumiel I., Grądzka I.
Nukleonika
|
2006
|
Vol. 51, nr 4
185-191
EN
Adaptive response (AR), an enhanced resistance to a high dose of ionising radiation acquired after pretreatment with a very low dose, was estimated in normal human lymphocytes. The question posed was whether the extent of radioadaptation, assessed by micronucleus test, would be related to the rate of DNA double-strand break (DSB) rejoining. Phytohemagglutinin-stimulated G1-lymphocytes from 5 healthy male volunteers were pre-treated (or not) with an adaptive (5 cGy) dose of X-rays, followed by a higher (5 or 10 Gy) challenge dose after 20-22 h. DSB rejoining after the challenge dose was monitored with the use of two methods: neutral comet assay, modified to reduce the contribution of single-strand breaks (SSBs) and thermolabile sites, and pulse-field gel electrophoresis (PFGE), specific for DSBs. At the level of micronuclei, an AR was observed in lymphocytes of 3 of 5 donors. Up to 60 min, comet assay showed no statistically significant differences in DNA break rejoining between adapted and non-adapted lymphocytes, independently of AR appearance. PFGE gave similar results, although in three donors it revealed secondary increases in DSBs levels at 30 min and/or 60 min post-irradiation in the adapted vs. the non-adapted samples. Failure to demonstrate changes in DSBs rejoining rate in the adapted lymphocytes could be due to diversity of AR intensity/timing at the level of DNA repair in not fully homogenous cell populations. Also, “rare” DNA cuts characteristic of early apoptosis/necrosis could overlap the process of DNA break rejoining.
19
Content available Concerted control of DNA double strand break repair and cell cycle progression in X-irradiated mammalian cells
Sochanowicz B., Szumiel I.
Nukleonika
|
2005
|
Vol. 50, nr 4
129-138
EN
Upon examination of cell cycle regulation in a damaged cell, relations were discovered of the cell cycle control mechanisms with a complicated web of signalling pathways, eventually called the genome surveillance system. After infliction of DNA double strand breaks (DSB), the signalling is initiated by sensor proteins and transducer protein kinase ATM. This kinase phosphorylates downstream effector proteins, such as checkpoint kinases CHK1 and CHK2, which initiate the pathways leading to cell cycle arrest. In contrast with the older model of linear transmission of signals in a certain sequence, it is now accepted that the damage signalling system is branched and contains feedback loops. DSB's presence is signalled by sensor proteins (MRE11-RAD50-nibrin complex, MRN) to ATM and the signal is amplified through adaptor proteins, MDC1/NFBD1 or 53BP1 (Tp53 binding protein). MRN contains a forkheadassociated (FHA) domain and BRCA1 carboxyl-terminal (BRCT) domain. The combination of the FHA/BRCT domains has a crucial role for the binding of nibrin to the H2AX histone, assembling the components of repair foci. These domains also are important for interaction of other proteins localised in the foci. For example, MDC1/NFBD1 contains a FHA domain and two BRCT domains which are involved in protein interactions. The signal generated at DSBs is amplified and transduced to recruit components of DNA repair systems. In a concerted way with the sequential recruitment of components of repair foci, activation of transcription of genes takes place, that is necessary for blocking progression through the cell cycle, for DNA repair or apoptosis.
20
Content available remote Efekt widza
Szumiel I.
Postępy Techniki Jądrowej
|
2004
|
z. 2
17-21
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