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  1. 19 Acta Biochimica Polonica

  2. 3 Open Chemistry

  3. 2 Biomonitoring

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  1. 4 Błasiak J.

  2. 3 Collins A. R.

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1
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Differences in basal DNA damage in blood cells from men and women

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Alija A. J., Collins A. R., Dreshaj S., Asllani F., Bajraktari I. D., Bresgen N., Eckl P. M.
Biomonitoring
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2016
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vol. 3
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issue 1
EN
We have recently shown that inhabitants of two polluted areas in Kosovo display more DNA damage (strand breaks in blood cell DNA) than do residents of a cleaner area. Here, we present additional analyses of these data and discuss additional data sets from Kosovo. Based on our data as well as the available data from other authors, age and sex-related differences in DNA damage or in susceptibility to DNA-damaging agents in the environment should be carefully considered when designing biomonitoring studies and when carrying out statistical analysis of the data.
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5',8-Cyclo-2'-deoxyadenosine (cdA) formation by γ-radiation. Theoretical quantum mechanics study

100%
Karwowski B., Grand A., Cadet J.
Acta Biochimica Polonica
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2009
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vol. 56
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issue 4
655-662
EN
Reactions of reactive oxygen species and more specifically - of hydroxyl radical (•OH) - with nucleosides may lead to the generation of radicals in the base and 2-deoxyribose moieties. In the present study emphasis was put on the possible reaction modes of 2'-deoxyadenosine (dA) radicals, leading to the formation of related 5',8-cyclonucleosides. It appears that the prerequisite for the formation of 5',8-cyclo-2'-deoxyadenosine (cdA) is the adoption of O4'-exo conformation by 2-deoxyribose; however, this is the least energetically favored conformer among the different puckered forms adopted by the furanose ring. The O4'-exo conformation was found to be present in each of the discussed mechanisms.
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Atmospheric pollution in Kosovo is associated with increased DNA damage in the human population

100%
Alija A. J., Asllani F., Bajraktari I. D., Collins A. R., Dreshaj S., Bresgen N., Eckl P. M.
Biomonitoring
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2015
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vol. 2
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issue 1
EN
In order to assess DNA damage associated with exposure to environmental pollution in two polluted sites and one control site in Kosovo, whole blood samples were collected from volunteers in two polluted areas (Kastriot/ Obiliq - lignite-based power plants and lignite mines - and Drenas/Gllogovc - Ferronikeli smelting plant) as well as from Peja, representing an unpolluted area. White blood cells were isolated, and DNA damage was analyzed by the alkaline comet assay. Significantly higher levels of DNA damage (strand breaks) were found in white blood cells from subjects living in the polluted areas compared with residents of the unpolluted city, indicating a potential threat to human health.
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A new look at adaptive mutations in bacteria.

100%
Janion C.
Acta Biochimica Polonica
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2000
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vol. 47
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issue 2
451-457
EN
This is a short survey of the adaptive mutation processes that arise in non- or slowly- dividing bacterial cells and includes: (i) bacterial models in which adaptive mutations are studied; (ii) the mutagenic lesions from which these mutations derive; (iii) the influence of DNA repair processes on the spectrum of adaptive mutations. It is proposed that in starved cells, likely as during the MFD phenomenon, lesions in tRNA suppressor genes are preferentially repaired and no suppressor tRNAs are formed as a result of adaptive mutations. Perhaps the most provocative proposal is (iv) a hypothesis that the majority of adaptive mutations are selected in a pre-apoptotic state where the cells are either mutated, selected, and survive, or they die.
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Age-dependent systemic DNA damage in early Type 2 Diabetes mellitus

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Rogulj D., El Aklouk I., Konjevoda P., Ljubić S., Pibernik Okanović M., Barbir A., Luburić M., Radman M., Budinski N., Vučić Lovrenčić M.
Acta Biochimica Polonica
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2017
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vol. 64
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issue 2
233-238
EN
Oxidative stress, capable of eliciting damage to various biomolecules including DNA, is a recognized component of diabetes mellitus and its complications. Metabolic syndrome (MetS) is associated with the development of type 2 diabetes mellitus (T2DM), as well as other unfavorable outcomes. The aim of this study was to elucidate the role of oxidative stress in the development of T2DM, by investigating association of oxidative DNA damage with metabolic parameters in subjects with MetS and early T2DM. Selected anthropometric and biochemical parameters of MetS, inflammation and oxidative DNA damage: body mass index (BMI), fatty liver index (FLI), waist circumference (WC), total cholesterol, HDL and LDL-cholesterol, gamma-glutamyl transpeptidase (GGT), uric acid, C-reactive protein (CRP), total leukocyte/neutrophil count, and urinary 8-hidroxy-deoxyguanosine (u-8-OHdG) were assessed in male subjects with MetS and both younger (≤55 years) and older (>55 years) subjects with T2DM of short duration without complications. BMI, FLI, WC, total and LDL-cholesterol and uric acid were higher, while the u-8-OHdG was lower in MetS group, when compared to older T2DM subjects. None of these parameters were different neither between MetS and younger T2DM, nor between two sub-groups of subjects with T2DM. Values of CRP, HDL-cholesterol, triglycerides, GGT, leukocytes and neutrophils were not different between all examined groups of subjects. Higher 8-OHdG in older subjects with T2DM suggests that both aging process and diabetes could contribute to the development of DNA damage. Oxidative DNA damage cannot serve as an universal early marker of T2DM.
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Detection of alkylation damage in human lymphocyte DNA with the comet assay.

100%
Collins A. R., Dušinská M., Horská A.
Acta Biochimica Polonica
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2001
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vol. 48
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issue 3
611-614
EN
The enzyme 3-methyladenine DNA glycosylase II (AlkA) is a bacterial repair enzyme that acts preferentially at 3-methyladenine residues in DNA, releasing the damaged base. The resulting baseless sugars are alkali-labile, and under the conditions of the alkaline comet assay (single cell gel electrophoresis) they appear as DNA strand breaks. AlkA is not lesion-specific, but has a low activity even with undamaged bases. We have tested the enzyme at different concentrations to find conditions that maximise detection of alkylated bases with minimal attack on normal, undamaged DNA. AlkA detects damage in the DNA of cells treated with low concentrations of methyl methanesulphonate. We also find low background levels of alkylated bases in normal human lymphocytes.Single cell gel electrophoresis (the comet assay) is widely used for the detection of strand breaks in nuclear DNA. It is particularly appropriate for studying the low background levels of damage present in normal human cells, such as peripheral lymphocytes. The cells are embedded in agarose on a microscope slide and lysed with Triton X-100 and 2.5 M NaCl, which remove cytoplasm and most nuclear proteins, but leave the DNA, in supercoiled form, as nucleoids. After incubation in alkali, the DNA is electrophoresed at high pH; DNA is drawn out to form a 'tail' (hence the name 'comet assay') - but only if breaks are present to relax the supercoiling of the nucleoid DNA. In order to increase its sensitivity and selectivity, we have incorporated into the assay an extra step in which the nucleoid DNA is digested with a lesion-specific endonuclease; the additional breaks revealed with this procedure indicate the presence of the particular lesion. So far, endonuclease III (NTH, specific for oxidised pyrimidines) (Collins et al., 1993), formamidopyrimidine DNA glycosylase (FPG, acting on ring-opened purines and the major purine oxidation produce, 8-oxoguanine) (Dušinská & Collins, 1996) and T4 endonuclease V (recognising UV-induced cyclobutane pyrimidine dimers) (Collins et al., 1997b) have been successfully employed. Amongst other things, we have estimated background levels of DNA oxidation (Collins et al., 1997a), and have found this damage to be elevated in human diseases such as diabetes and ankylosing spondylitis (Dušinská et al., 1999).We now report the use of AlkA, a bacterial repair enzyme whose main substrate is 3-methyladenine in DNA, though it also recognises - with lower efficiency - other modified bases (Lindahl, 1993). A recent report (Berdal et al., 1998) suggests that repair enzymes supposedly specific for alkylated bases may in fact create breaks non-selectively (though much less efficiently) at normal bases. Given the size of the genome, even a low efficiency of non-specific breakage could significantly interfere in estimations of background levels of alkylation damage. We reasoned that, by employing a range of concentrations of the enzyme, and carrying out incubations for different lengths of time, we might find a concentration at which only the alkylated bases would be detected, so that the number of breaks would increase to a certain level and then plateau. After optimising reaction conditions, we tested the assay on lymphocytes from different individuals, and also, as a positive control, examined alkylation damage induced by methyl methanesulphonate.
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Ionisation potential and electron affinity of free 5′,8-cyclopurine-2′-deoxynucleosides. DFT study in gaseous and aqueous phase

88%
Karwowski B.
Open Chemistry
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2010
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vol. 8
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issue 1
70-76
EN
Oxidatively generated damage to DNA frequently appears in the human genome as an effect of aerobic metabolism or as the result of exposure to exogenous oxidizing agents. Due to these facts it was decided to present, for the first time, the electron affinity, ionization potential of 5′,8-cyclo-2′-deoxyadenosine/guanosine (cdA, cdG) in their 5′R and 5′S diastereomeric forms. For all points of quantum mechanics studies presented, the density functional theory (DFT) with B3LYP parameters on 6-311++G** basis set level was used. The zero-point vibrational corrected adiabatic electron affinity (AEA) and adiabatic ionization potential (AIP) were calculated. Additionally the vertical electron affinity (VEA), vertical detachment energy (VDE) and vertical ionization potential were taken into consideration. AEA in eV (gaseous/aqueous phase) are as follows: 0.3/1.81 (5′R)cdA, 0.13/1.76 (5′S)cdA, 0.17/1.49 (5′R)cdG, 0.14/1.53 (5′S)cdG and AIP followed the order 7.43/5.59(5′S)cdG, 7.49/5.60(5′R)cdG, 7.77/5.97(5′R)cdA, 7.84/5.93(5′S)cdA. The obtained AIPs were found to be lower than that for corresponding natural nucleosides. Therefore, even though the 5′,8-cyclopurine-2′-deoxynucleoside level in a cell was judged as low, they can play an important role in the stability, replication and transcription of genes. [...]
8
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Dna Damage in Crepis Capillaris Cells in Response to in Vitro Conditions

88%
Nawrocki W., Siwińska D., Kwasniewska J., Maluszynska J.
Acta Biologica Cracoviensia s. Botanica
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2012
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vol. 54
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issue 2
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DNA-based biosensors with external Nafion and chitosan membranes for the evaluation of the antioxidant activity of beer, coffee, and tea

88%
Hlavatá L., Vyskočil V., Beníková K., Borbélyová M., Labuda J.
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issue 5
604-611
EN
Novel electrochemical DNA-based biosensors with outer-sphere Nafion and chitosan protective membranes were prepared for the evaluation of antioxidant properties of beverages (beer, coffee, and black tea) against prooxidant hydroxyl radicals. A carbon working electrode of a screen-printed three-electrode assembly was modified using a layer-by-layer deposition technique with low molecular weight double-stranded DNA and a Nafion or chitosan film. The membrane-covered DNA biosensors were initially tested with respect to their voltammetric and impedimetric response after the incubation of the beverage and the medium exchange for the solution of the redox indicator [Fe(CN)6]3−/4−. While the Nafion-protected biosensor proved to be suitable for beer and black tea extracts, the chitosan-protected biosensor was successfully used in a coffee extract. Afterwards, the applicability was successfully verified for these biosensors for the detection of a deep degradation of the surface-attached DNA at the incubation in the cleavage agent (hydroxyl radicals generated via Fenton reaction) and for the evaluation of antioxidant properties of coffee and black tea extracts against prooxidant hydroxyl radicals. The investigation of the novel biosensors with a protective membrane represents a significant contribution to the field of electrochemical DNA biosensors utilization.
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The influence of the phosphorothioate diester bond on the DNA oxidation process

88%
Karwowski B. T.
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issue 1
EN
This study describes the influence of the phosphorothioate internucleotide bond on the deoxyribonucleic acid (DNA) oxidation process. The interaction of an ultraviolet radiation (UVA) with a targeted double-stranded (ds) oligonucleotide, in which one strand contains an antraquinone (AQ) moiety on the 5’-end, may lead to a hole migration process through the double helix. In the end, the migration of theformed radical cation terminates in a suitable place. Usually, this is a guanine-rich sequence. In another experiment, phosphorothioate internucleotide bonds were detected in the bacterial genome as a natural modification. In this study, a polyacrylamide gel electrophoresis (PAGE) autoradiogram analysis of irradiated ds-DNA showed that the oxidation reaction was not inhibited by an isolated guanine. Instead, irrespective of the absence or presence of a phosphorothioate bond, the termination of the ds-DNA oxidation process was predominantly observed on the thymine moieties. Based on the obtained results, it can be concluded that in the discussed case, a hole migration by a hopping mechanism is in competition with an oxidation reaction with a superoxide radical anion. Alternatively, the radical cation migration process is sequence-dependent due to its different ionization potentials. Therefore, the presence of a phosphorothioate internucleotide bond did not change the stability of ds-DNA under UVA irradiation conditions.
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Protective action of vitamin C against DNA damage induced by selenium-cisplatin conjugate.

75%
Błasiak J., Kowalik J.
Acta Biochimica Polonica
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2001
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vol. 48
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issue 1
233-240
EN
Genotoxicity of anticancer drugs is of a special interest due to the risk of inducing secondary malignancies. Vitamin C (ascorbic acid) is a recognized antioxidant and, since human diet can be easily supplemented with vitamin C, it seems reasonable to check whether it can protect against DNA-damaging effects of antitumor drugs. In the present work the ability of vitamin C to modulate cytotoxic and genotoxic effects of a cisplatin analog, conjugate (NH3)2Pt(SeO3), in terms of cell viability, DNA damage and repair in human lymphocytes was examined using the trypan blue exclusion test and the alkaline comet assay, respectively. The conjugate evoked a concentration-dependent decrease in the cell viability, reaching nearly 50% at 250 μM. (NH3)2Pt(SeO3) at 1, 10 and 30 μM caused DNA strand breaks, measured as the increase in the comet tail moment of the lymphocytes. The treated cells were able to recover within a 30-min incubation in a drug-free medium at 37°C. Vitamin C at 10 and 50 μM diminished the extent of DNA damage evoked by (NH3)2Pt(SeO3) but had no effect on the kinetics of DNA repair. The vitamin did not directly inactivate the conjugate. Lymphocytes treated with endonuclease III, which recognises oxidised pyrimidines, displayed a greater tail moment than those untreated with the enzyme, suggesting that the damages induced by the drug have, at least in part, an oxidative origin. Vitamin C can be considered a potential protective agent against side effects of antitumor drugs, but further research with both normal and cancer cells are needed to clarify this point.
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A comparison of the in vitro genotoxicity of anticancer drugs idarubicin and mitoxantrone.

75%
Błasiak J., Gloc E., Warszawski M.
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vol. 49
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issue 1
145-155
EN
Idarubicin is an anthracycline antibiotic used in cancer therapy. Mitoxantrone is an anthracycline analog with presumed better antineoplastic activity and lesser toxicity. Using the alkaline comet assay we showed that the drugs at 0.01-10 μM induced DNA damage in normal human lymphocytes. The effect induced by idarubicin was more pronounced than by mitoxantrone (P < 0.001). The cells treated with mitoxantrone at 1 μM were able to repair damage to their DNA within a 30-min incubation, whereas the lymphocytes exposed to idarubicin needed 180 min. Since anthracyclines are known to produce free radicals, we checked whether reactive oxygen species might be involved in the observed DNA damage. Catalase, an enzyme inactivating hydrogen peroxide, decreased the extent of DNA damage induced by idarubicin, but did not affect the extent evoked by mitoxantrone. Lymphocytes exposed to the drugs and treated with endonuclease III or formamidopyrimidine-DNA glycosylase (Fpg), enzymes recognizing and nicking oxidized bases, displayed a higher level of DNA damage than the untreated ones. 3-Methyladenine-DNA glycosylase II (AlkA), an enzyme recognizing and nicking mainly methylated bases in DNA, increased the extent of DNA damage caused by idarubicin, but not that induced by mitoxantrone. Our results indicate that the induction of secondary malignancies should be taken into account as side effects of the two drugs. Direct strand breaks, oxidation and methylation of the DNA bases can underlie the DNA-damaging effect of idarubicin, whereas mitoxantrone can induce strand breaks and modification of the bases, including oxidation. The observed in normal lymphocytes much lesser genotoxicity of mitoxantrone compared to idarubicin should be taken into account in planning chemotherapeutic strategies.
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Changes in phosphorylation of histone H2A.X and p53 in response of peripheral blood lymphocytes to gamma irradiation

75%
Vilasová Z., Řezáčová M., Vávrová J., Tichý A., Vokurková D., Zoelzer F., Řeháková Z., Osterreicher J., Lukášová E.
Acta Biochimica Polonica
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2008
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vol. 55
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issue 2
381-390
EN
The main aim of this study was to compare the reaction of quiescent and proliferating, i.e. phytohemagglutinin (PHA)-stimulated, human peripheral blood mononuclear cells (PBMCs) to γ-radiation, and analyse changes of proteins related to repair of DNA damage and apoptosis, such as γH2A.X, p53, p53 phosphorylation at serines-15 and -392, and p21 and their dose dependence. Freshly isolated PBMCs in peripheral blood are predominantly quiescent, in G0 phase, and with very low amounts of proteins p53 and p21. Using confocal microscopy we detected dose dependent (0.5-5 Gy) induction of foci containing γH2A.X (1 h after γ-ray exposure), which are formed around radiation-induced double strand breaks of DNA. Apoptosis was detected from 24 h after irradiation by the dose of 4 Gy onwards by Annexin V binding and lamin B cleavage. Seventy two hours after irradiation 70% of CD3+ lymphocytes were A+. Neither increase in p53 nor its phosphorylation on serine-392 after irradiation was detected in these cells. However, massive increase in p21 (cyclin-dependent kinase inhibitor 1A) was detected after irradiation, which can be responsible for late occurrence of apoptosis in these quiescent cells. PHA-stimulation itself (72 h) caused an increase in early apoptosis (A+PI-) in comparison to non-stimulated PBMCs (38% A+ resp. 13.4%). After PHA-stimulation also the amount of γH2A.X, p53, and p21 increased, but no phosphorylation of p53 on serine-392 or -15 was detected. Reaction to γ-radiation was different in PHA-stimulated lymphocytes: the p53 pathway was activated and p53 was phosphorylated on serines-15 and -392 4 h after irradiation by the dose of 4 Gy. Phosphorylation of p53 at serine-15 increased in a dose-dependent manner in the studied dose range 0.2-7.5 Gy. Also the amount of p21 increased after irradiation. Seventy two hours after irradiation of PHA-stimulated CD3+ T lymphocytes by the dose of 4 Gy 65% of cells were A+.
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Evaluation of DNA damage in white blood cells of healthy human volunteers using the alkaline comet assay and the chromosome aberration test

75%
Kopjar N., Želježić D., Garaj-Vrhovac V.
Acta Biochimica Polonica
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2006
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vol. 53
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issue 2
321-336
EN
The present study was undertaken to contribute to the characterization of the degree of variability in baseline damage in white blood cells from control population, and to investigate how this variability is associated with external and internal factors. Altogether 170 healthy volunteers, randomly selected from the general population of the Republic of Croatia, participated in the study. Two sensitive tests: the alkaline comet assay and the chromosome aberration test were applied to study the background levels of DNA damage in their white blood cells. The results point to inter-individual differences, indicating different genome sensitivity. As revealed by both assays, the background levels of DNA damage were mostly influenced by smoking habit as well as medical exposure (especially to diagnostic X-rays). Sex and age of subjects did not significantly influence the values of DNA damage recorded in the white blood cells. Although higher levels of DNA damage were recorded in blood samples collected during winter and autumn, they were mostly influenced by medicinal exposure and smoking habit. Statistical evaluation of the data confirmed that a positive correlation exists between DNA migration and the number of long-tailed nuclei found with the comet assay and the total number of chromosome aberrations. The data obtained can serve as control values in forthcoming biomonitoring studies.
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Correlation between folate and vitamin B12 and markers of DNA stability in healthy men: preliminary results

75%
Milić M., Rozgaj R., Kašuba V., Oreščanin V., Balija M., Jukić I.
Acta Biochimica Polonica
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2010
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vol. 57
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issue 3
339-345
EN
The aim of this study was to find correlations between folate and vitamin B12 on baseline damage in white blood cells and their association with smoking, alcohol consumption and ageing. Thirty-six healthy vitamin non-deficient male subjects were selected in a randomized study. Comet assay (SCGE) and micronucleus (MN) assay were used as biomarkers of DNA damage. The amount of DNA damage was correlated with vitamin B12 and folic acid concentration. Positive, but non-significant correlation (canonical R = 0.61; χ2=28.97; P=0.253) was found between micronucleus (MN) frequency or comet assay parameters (SCGE) and five covariates (age, smoking, alcohol consumption, vitamin B12 and folate blood serum concentration). The highest MN frequency was observed in the group with the lowest vitamin B12 concentration (F=3.59; P=0.024). The SCGE assay failed to show significant correlation with vitamin B12 or folic acid concentration. Concentration of vitamin B12 was significantly correlated with incidence of micronuclei. Our results present background data that could be valuable for future genotoxicological monitoring.
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High levels of bulky DNA adducts in human sperm correlate with impaired fertility.

75%
Horak S., Polańska J., Widłak P.
Acta Biochimica Polonica
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2003
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vol. 50
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issue 1
197-203
EN
Progressive decline in fertility and sperm quality has been reported over the last few decades, especially in industrialized nations. It has been proposed that exposure to factors that induce damage in DNA of spermatogenic cells may significantly contribute to impaired fertility. Here, the 32P-postlabelling method was used to analyze the levels of bulky DNA adducts in sperm cells in a group of 179 volunteers, either healthy subjects or patients with an impaired fertility. The levels of DNA adducts were 1.35-fold higher in the infertile group as compared to healthy individuals (P = 0.012). Similarly, a significant negative correlation between the levels of DNA adducts and measures of semen quality (sperm concentration and motility) has been observed (P Ł 0.001). In addition, the levels of bulky DNA adducts in sperm cells positively correlates with amounts of leukocytes in semen, which were significantly higher in semen of infertile subjects.
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TEL/JAK2 tyrosine kinase inhibits DNA repair in the presence of amifostine.

75%
Gloc E., Warszawski M., Młynarski W., Stolarska M., Hoser G., Skorski T., Błasiak J.
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vol. 49
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issue 1
121-128
EN
The TEL/JAK2 chromosomal translocation (t(9;12)(p24;p13)) is associated with T cell childhood acute lymphoblastic leukemia. The TEL/JAK2 fusion protein contains the JAK2 catalytic domain and the TEL-specific oligomerization domain. TEL-mediated oligomerization of the TEL/JAK2 proteins results in the constitutive activation of the tyrosine kinase activity. Leukemia cells expressing TEL/JAK2 tyrosine kinase become resistant to anti-neoplastic drugs. Amifostine is a pro-drug which can selectively protect normal tissues against the toxicity of anticancer drugs and radiation. investigated the effects of amifostine on idarubicin-induced DNA damage and repair in murine pro-B lymphoid BaF3 cells and BaF3-TEL/JAK2-transformed cells using alkaline single cell gel electrophoresis (comet assay). Idarubicin induced DNA damage in both cell types but amifostine reduced its extent in control non-transformed BaF3 cells and enhanced it in TEL/JAK2-transformed cells. The transformed cells did not show measurable DNA repair after exposure to amifostine and idarubicin, but cells treated only with idarubicin were able to recover within a 60-min incubation. Because TEL/JAK2-transformed cells can be considered as model cells for certain human leukemias and lymphomas we anticipate an enhancement of idarubicin cytotoxicity by amifostine in these diseases. Moreover, TEL/JAK2 tyrosine kinase might be involved in cellular response to DNA damage. Amifostine could promote apoptosis or lower the threshold for apoptosis induction dependent on TEL/JAK2 activation.
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Bacterial DNA repair genes and their eukaryotic homologues: 4. The role of nucleotide excision DNA repair (NER) system in mammalian cells

75%
Maddukuri L., Dudzińska D., Tudek B.
Acta Biochimica Polonica
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2007
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vol. 54
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issue 3
469-482
EN
The eukaryotic cell encounters more than one million various kinds of DNA lesions per day. The nucleotide excision repair (NER) pathway is one of the most important repair mechanisms that removes a wide spectrum of different DNA lesions. NER operates through two sub pathways: global genome repair (GGR) and transcription-coupled repair (TCR). GGR repairs the DNA damage throughout the entire genome and is initiated by the HR23B/XPC complex, while the CSB protein-governed TCR process removes DNA lesions from the actively transcribed strand. The sequence of events and the role of particular NER proteins are currently being extensively discussed. NER proteins also participate in other cellular processes like replication, transcription, chromatin maintenance and protein turnover. Defects in NER underlay severe genetic disorders: xeroderma pigmentosum (XP), Cockayne syndrome (CS) and trichothiodystrophy (TTD).
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DNA damage and repair in lymphocytes of normal individuals and cancer patients: studies by the comet assay and micronucleus tests.

75%
Palyvoda O., Polańska J., Wygoda A., Rzeszowska-Wolny J.
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EN
A population study is reported in which the DNA damage induced by γ-radiation (2 Gy) and the kinetics of the subsequent repair were estimated by the comet and micronucleus assays in isolated lymphocytes of 82 healthy donors and patients with head and neck cancer before radiotherapy. The parameters of background and radiation-induced DNA damage, rate of repair, and residual non-repaired damage were measured by comet assay, and the repair kinetics for every donor were computer-fitted to an exponential curve. The level of background DNA damage before irradiation measured by comet assay as well as the level of micronuclei were significantly higher in the head and neck cancer patient group than in the healthy donors, while the parameters of repair were widely scattered in both groups. Cancer patient group contained significantly more individuals, whose irradiated lymphocytes showed high DNA damage, low repair rate and high non-repaired DNA damage level. Lymphocytes of donors belonging to this subgroup showed significantly lower inhibition of cell cycle after irradiation.
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Content available

Reactive oxygen species in BCR-ABL1-expressing cells - relevance to chronic myeloid leukemia

75%
Antoszewska-Smith J., Pawlowska E., Blasiak J.
Acta Biochimica Polonica
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2017
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vol. 64
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issue 1
1-10
EN
Chronic myeloid leukemia (CML) results from the t(9;22) reciprocal chromosomal translocation producing the BCR-ABL1 gene, conferring growth and proliferation advantages in the CML cells. CML progresses from chronic, often syndrome-free, to blast phase, fatal if not treated. Although the involvement of BCR-ABL1 in some signaling pathways is considered as the cause of CML, the mechanisms resulting in its progression are not completely known. However, BCR-ABL1 stimulates the production of reactive oxygen species (ROS), which levels increase with CML progression and induce BCR-ABL1 self-mutagenesis. Introducing imatinib and other tyrosine kinase inhibitors (TKIs) to CML therapy radically improved its outcome, but TKIs-resistance became an emerging problem. TKI resistance can be associated with even higher ROS production than in TKI-sensitive cells. Therefore, ROS-induced self-mutagenesis of BCR-ABL1 can be crucial for CML progression and TKI resistance and in this way should be taken into account in therapeutic strategies. As a continuous production of ROS by BCR-ABL1 would lead to its self-destruction and death of CML cells, there must be mechanisms controlling this phenomenon. These can be dependent on DNA repair, which is modulated by BCR-ABL1 and can be different in CML stem and progenitor cells. Altogether, the mechanisms of the involvement of BCR-ABL1 in ROS signaling can be engaged in CML progression and TKI-resistance and warrant further study.
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