Search results

1

Detection of alkylation damage in human lymphocyte DNA with the comet assay.

100%

Collins A. R., Dušinská M., Horská A.

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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.

2

5',8-Cyclo-2'-deoxyadenosine (cdA) formation by γ-radiation. Theoretical quantum mechanics study

100%

Karwowski B., Grand A., Cadet J.

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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.

3

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.

4

A new look at adaptive mutations in bacteria.

100%

Janion C.

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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.

5

Age-dependent systemic DNA damage in early Type 2 Diabetes mellitus

100%

Rogulj D., El Aklouk I., Konjevoda P., Ljubić S., Pibernik Okanović M., Barbir A., Luburić M., Radman M., Budinski N., Vučić Lovrenčić M.

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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.

6

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

100%

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.

7

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

8

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.

Open Chemistry

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2014

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vol. 12

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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.

9

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. [...]

10

The influence of the phosphorothioate diester bond on the DNA oxidation process

88%

Karwowski B. T.

Open Chemistry

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2015

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vol. 13

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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.

11

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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2002

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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.

12

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.

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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).

13

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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2003

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vol. 50

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issue 1

181-190

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.

14

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

75%

Antoszewska-Smith J., Pawlowska E., Blasiak J.

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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.

15

Bacterial DNA repair genes and their eukaryotic homologues: 2. Role of bacterial mutator gene homologues in human disease. Overview of nucleotide pool sanitization and mismatch repair systems

75%

Arczewska K. D., Kuśmierek J. T.

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2007

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vol. 54

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issue 3

435-457

EN

Since the discovery of the first E. coli mutator gene, mutT, most of the mutations inducing elevated spontaneous mutation rates could be clearly attributed to defects in DNA repair. MutT turned out to be a pyrophosphohydrolase hydrolyzing 8-oxodGTP, thus preventing its incorporation into DNA and suppresing the occurrence of spontaneous AT→CG transversions. Most of the bacterial mutator genes appeared to be evolutionarily conserved, and scientists were continuously searching for contribution of DNA repair deficiency in human diseases, especially carcinogenesis. Yet a human MutT homologue - hMTH1 protein - was found to be overexpressed rather than inactivated in many human diseases, including cancer. The interest in DNA repair contribution to human diseases exploded with the observation that germline mutations in mismatch repair (MMR) genes predispose to hereditary non-polyposis colorectal cancer (HNPCC). Despite our continuously growing knowledge about DNA repair we still do not fully understand how the mutator phenotype contributes to specific forms of human diseases.

16

Dynamics of estrogen-induced oxidative stress

75%

Kobiela J., Stefaniak T., Krajewski J., Kalinska-Blach B., Zurawa-Janicka D., Lachinski A., Gackowski D., Olinski R., Nowak J., Knap N., Lipinska B., Sledzinski Z., Wozniak M.

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2007

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vol. 54

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issue 2

289-295

EN

The objective of this study was to assess the dynamics of oxidative damage to cellular macromolecules such as proteins, lipids and DNA under conditions of oxidative stress triggering early stages of estrogen-dependent carcinogenesis. A rodent model of carcinogenesis was used. Syrian hamsters were sacrificed after 1, 3, 5 h and one month from the initial implantation of estradiol. Matching control groups were used. Kidneys as target organs for estradiol-mediated oxidative stress were excised and homogenized for biochemical assays. Subcellular fractions were isolated. Carbonyl groups (as a marker of protein oxidation) and lipid hydroxyperoxides were assessed. DNA was isolated and 8-oxodGuo was assessed. Electron paramagnetic resonance spectroscopy was used to confirm the results for lipid peroxidation. Exposition to estradiol in the rodent model leads to damage of macromolecules of the cell, including proteins and DNA, but not lipids. Proteins appear to be the primary target of the damage but are closely followed by DNA. It has previously been speculated that protein peroxides can increase DNA modifications. This time sequence was observed in our study. Nevertheless, the direct relation between protein and DNA damage still remains unsolved.

17

Recognition and repair of DNA-cisplatin adducts.

75%

Woźniak K., Błasiak J.

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2002

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vol. 49

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issue 3

583-596

EN

Anticancer activity of cisplatin (cis-diamminedichloroplatinum) is believed to result from its interaction with DNA. The drug reacts with nucleophilic sites in DNA forming monoadducts as well as intra- and interstrand crosslinks. DNA-cisplatin adducts are specifically recognized by several proteins. They can be divided into two classes. One constitutes proteins which recognize DNA damage as an initial step of the nucleotide excision and mismatch repair pathways. The other class contains proteins stabilizing cellular DNA-protein and protein-protein complexes, including non-histone proteins from the HMG (high-mobility-group) family. They specifically recognize 1,2-interstrand d(GpG) and d(ApG) crosslinks of DNA-cisplatin adducts and inhibit their repair. Many HMG-domain proteins can function as transcription factors, e.g. UBF, an RNA polymerase I transcription factor, the mammalian testis-determining factor SRY and the human mitochondrial transcription factor mtTFA. Moreover, it seems that some proteins, which probably recognize DNA-cisplatin adducts non-specifically, e.g. actin and other nuclear matrix proteins, can disturb the structural and functional organization of the nucleus and whole cell. The formation of complexes between DNA and proteins in the presence of cisplatin and the changes in the cell architecture may account for the drug cytotoxicity.

18

Molecular mechanisms of lead toxicity

75%

SZYMAŃSKI M.

BioTechnologia

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2014

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vol. 95

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issue 2

137-149

EN

Lead is a ubiquitous xenobiotic metal and because of its widespread industrial use is one of the most serious environmental pollutants. Lead is highly toxic and exposure to even low doses can produce adverse effects on all living organisms. In humans, lead exposure can affect virtually all body systems, resulting in severe health problems. On a molecular level, lead can alter or interfere with the activity of proteins and nucleic acids, ultimately resulting in changes in cell metabolism and physiology leading to pathologic states. Lead can also affect the functions of macromolecules, directly or indirectly, by inducing oxidative stress, which is regarded as a primary factor in pathophysiology of lead exposure.

19

A comparison of the in vitro genotoxicity of anticancer drugs idarubicin and mitoxantrone.

75%

Błasiak J., Gloc E., Warszawski M.

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2002

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vol. 49

|

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.

20

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.

|

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.

Refine search results

Detection of alkylation damage in human lymphocyte DNA with the comet assay.

5',8-Cyclo-2'-deoxyadenosine (cdA) formation by γ-radiation. Theoretical quantum mechanics study

Atmospheric pollution in Kosovo is associated with increased DNA damage in the human population

A new look at adaptive mutations in bacteria.

Age-dependent systemic DNA damage in early Type 2 Diabetes mellitus

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

Dna Damage in Crepis Capillaris Cells in Response to in Vitro Conditions

DNA-based biosensors with external Nafion and chitosan membranes for the evaluation of the antioxidant activity of beer, coffee, and tea

Ionisation potential and electron affinity of free 5′,8-cyclopurine-2′-deoxynucleosides. DFT study in gaseous and aqueous phase

The influence of the phosphorothioate diester bond on the DNA oxidation process

TEL/JAK2 tyrosine kinase inhibits DNA repair in the presence of amifostine.

Bacterial DNA repair genes and their eukaryotic homologues: 4. The role of nucleotide excision DNA repair (NER) system in mammalian cells

DNA damage and repair in lymphocytes of normal individuals and cancer patients: studies by the comet assay and micronucleus tests.

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

Bacterial DNA repair genes and their eukaryotic homologues: 2. Role of bacterial mutator gene homologues in human disease. Overview of nucleotide pool sanitization and mismatch repair systems

Dynamics of estrogen-induced oxidative stress

Recognition and repair of DNA-cisplatin adducts.

Molecular mechanisms of lead toxicity

A comparison of the in vitro genotoxicity of anticancer drugs idarubicin and mitoxantrone.

Evaluation of DNA damage in white blood cells of healthy human volunteers using the alkaline comet assay and the chromosome aberration test