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Tytuł:
Comparison of the effects of bleomycin and ionizing radiation in two sublines of murine lymphoma L5178Y
Autorzy:
Kruszewski, M.
Zaim, J.
Grądzka, I.
Szumiel, I.
Powiązania:
https://bibliotekanauki.pl/articles/147561.pdf
Data publikacji:
2001
Wydawca:
Instytut Chemii i Techniki Jądrowej
Tematy:
bleomycin
comet assay
DNA damage
gamma radiation
single cell gel electrophoresis
Opis:
We compared the effects of bleomycin (BLM) and ionizing radiation on two sublines of murine lymphoma L5178Y (LY): LY-R, radiation resistant and LY-S, radiation sensitive. This radiosensitivity difference is related to the ability to rejoin DNA double strand breaks. LY-S cells were about two times more sensitive to BLM than LY-R, similarly as in the case of sensitivity to X rays. Since there was no difference in the P-glycoprotein-related drug transport system between the sublines, it could be expected that the enhanced sensitivity of LY-S cells to BLM was caused by the DNA repair defect. Growth disturbances in BLM treated cell populations were proportional to the lethal effect and their duration was observed until elimination of dead cells (3-6 days after 50 ěM BLM, 1 h at 37oC). There was no slow growth phase accompanied by normal viability, as previously described for X-irradiated LY-S cells. Initial DNA damage, estimated with the single cell gel electrophoresis method was linearly related to BLM dose in LY-S cells; in LY-R cells - in the low dose range (up to 10 ěM) - there was more damage than in LY-S cells, however, at higher doses the dose - effect curves became identical. The doseeffect relationship for ă rays was linear and identical in both cell sublines. DNA damage distribution in BLM treated cells was much less uniform as compared to that in irradiated cells and indicated the presence of cells with severely damaged DNA, a feature typical for BLM action in vitro.
Źródło:
Nukleonika; 2001, 46, 3; 81-86
0029-5922
1508-5791
Pojawia się w:
Nukleonika
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Detection of alkylation damage in human lymphocyte DNA with the comet assay.
Autorzy:
Collins, Andrew
Dušinská, Mária
Horská, Alexandra
Powiązania:
https://bibliotekanauki.pl/articles/1044089.pdf
Data publikacji:
2001
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
AlkA
DNA damage
comet assay
Opis:
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.
Źródło:
Acta Biochimica Polonica; 2001, 48, 3; 611-614
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Protective action of vitamin C against DNA damage induced by selenium-cisplatin conjugate.
Autorzy:
Błasiak, Janusz
Kowalik, Joanna
Powiązania:
https://bibliotekanauki.pl/articles/1044192.pdf
Data publikacji:
2001
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
endonuclease III
vitamin C
Se-Pt conjugate [(NH3)2Pt(SeO3)]
genotoxic effects of anticancer drugs
DNA damage
comet assay
DNA repair
Opis:
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.
Źródło:
Acta Biochimica Polonica; 2001, 48, 1; 233-240
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
A comparison of the in vitro genotoxicity of anticancer drugs idarubicin and mitoxantrone.
Autorzy:
Błasiak, Janusz
Gloc, Ewa
Warszawski, Mariusz
Powiązania:
https://bibliotekanauki.pl/articles/1043821.pdf
Data publikacji:
2002
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
mitoxantrone
oxidative DNA damage
DNA damage
idarubicin
comet assay
DNA methylation
DNA repair
Opis:
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.
Źródło:
Acta Biochimica Polonica; 2002, 49, 1; 145-155
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Modified neutral comet assay for human lymphocytes
Autorzy:
Wojewódzka, M.
Grądzka, I.
Buraczewska, I.
Powiązania:
https://bibliotekanauki.pl/articles/147130.pdf
Data publikacji:
2002
Wydawca:
Instytut Chemii i Techniki Jądrowej
Tematy:
DNA double strand breaks
human lymphocyte
neutral comet assay
Opis:
Comet assay under neutral conditions allows the detection of DNA double-strand breaks, considered to be the biologically relevant radiation-induced lesion. In this report we describe modifications of the neutral comet method, which simplify and facilitate its use for estimation of DNA double strand breaks in human lymphocytes irradiated with doses of 60Co gamma-rays (from 10 to 100 Gy). The analysis carried out according to this protocol takes less time than those published so far. Also, the use of lysis at 50°C is avoided; this is important in view of the presence of heat-labile sites in the DNA of irradiated cells, recently reported by Rydberg [12]. The comets have well defined, sharp limits, are suitable for computer image analysis and chromatin of the control cells remains condensed.
Źródło:
Nukleonika; 2002, 47, 1; 1-5
0029-5922
1508-5791
Pojawia się w:
Nukleonika
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
TEL/JAK2 tyrosine kinase inhibits DNA repair in the presence of amifostine.
Autorzy:
Gloc, Ewa
Warszawski, Mariusz
Młynarski, Wojciech
Stolarska, Małgorzata
Hoser, Grażyna
Skorski, Tomasz
Błasiak, Janusz
Powiązania:
https://bibliotekanauki.pl/articles/1043817.pdf
Data publikacji:
2002
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
oncogenic tyrosine kinase
amifostine
DNA damage
idarubicin
comet assay
DNA repair
TEL/JAK2
Opis:
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.
Źródło:
Acta Biochimica Polonica; 2002, 49, 1; 121-128
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
DNA damage and repair in lymphocytes of normal individuals and cancer patients: studies by the comet assay and micronucleus tests.
Autorzy:
Palyvoda, Olena
Polańska, Joanna
Wygoda, Andrzej
Rzeszowska-Wolny, Joanna
Powiązania:
https://bibliotekanauki.pl/articles/1043662.pdf
Data publikacji:
2003
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
ionizing radiation
DNA damage
human lymphocytes
comet assay
head and neck tumors
DNA repair
Opis:
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.
Źródło:
Acta Biochimica Polonica; 2003, 50, 1; 181-190
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Free radical scavengers can modulate the DNA-damaging action of alloxan.
Autorzy:
Blasiak, Janusz
Sikora, Agnieszka
Czechowska, Agnieszka
Drzewoski, Józef
Powiązania:
https://bibliotekanauki.pl/articles/1043667.pdf
Data publikacji:
2003
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
vitamin C
spin trapping
free radicals
alloxan
vitamin E
DNA damage
ebselen
comet assay
DNA repair
diabetes mellitus
Opis:
Alloxan can generate diabetes in experimental animals and its action can be associated with the production of free radicals. It is therefore important to check how different substances often referred to as free radical scavengers may interact with alloxan, especially that some of these substance may show both pro- and antioxidant activities. Using the alkaline comet assay we showed that alloxan at concentrations 0.01-50 μM induced DNA damage in normal human lymphocytes in a dose-dependent manner. Treated cells were able to recover within a 120-min incubation. Vitamins C and E at 10 and 50 μM diminished the extent of DNA damage induced by 50 μM alloxan. Pre-treatment of the lymphocytes with a nitrone spin trap, α-(4-pyridil-1-oxide)- N-t-butylnitrone (POBN) or ebselen (2-phenyl-1,2-benzisoselenazol-3(2H)-one), which mimics glutathione peroxides, reduced the alloxan-evoked DNA damage. The cells exposed to alloxan and treated with formamidopyrimidine-DNA glycosylase (Fpg) and 3-methyladenine-DNA glycosylase II (AlkA), enzymes recognizing oxidized and alkylated bases, respectively, displayed greater extent of DNA damage than those not treated with these enzymes. The results confirmed that free radicals are involved in the formation of DNA lesions induced by alloxan. The results also suggest that alloxan can generate oxidized DNA bases with a preference for purines and contribute to their alkylation.
Źródło:
Acta Biochimica Polonica; 2003, 50, 1; 205-210
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Labile iron pool correlates with iron content in the nucleus and the formation of oxidative DNA damage in mouse lymphoma L5178Y cell lines.
Autorzy:
Kruszewski, Marcin
Iwaneńko, Teresa
Powiązania:
https://bibliotekanauki.pl/articles/1043668.pdf
Data publikacji:
2003
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
iron homeostasis
hydrogen peroxide
comet assay
Opis:
Labile iron pool (LIP) constitutes a crossroad of metabolic pathways of iron-containing compounds and is midway between the cellular need for iron, its uptake and storage. In this study we investigated oxidative DNA damage in relation to the labile iron pool in a pair of mouse lymphoma L5178Y (LY) sublines (LY-R and LY-S) differing in sensitivity to hydrogen peroxide. The LY-R cells, which are hydrogen peroxide-sensitive, contain 3 times more labile iron than the hydrogen peroxide-resistant LY-S cells. Using the comet assay, we compared total DNA breakage in the studied cell lines treated with hydrogen peroxide (25 μM for 30 min at 4°C). More DNA damage was found in LY-R cells than in LY-S cells. We also compared the levels of DNA lesions sensitive to specific DNA repair enzymes in both cell lines treated with H2O2. The levels of endonuclease III-sensitive sites and Fapy-DNA glycosylase-sensitive sites were found to be higher in LY-R cells than in LY-S cells. Our data suggest that the sensitivity of LY-R cells to H2O2 is partially caused by the higher yield of oxidative DNA damage, as compared to that in LY-S cells. The critical factor appears to be the availability of transition metal ions that take part in the OH radical-generating Fenton reaction (very likely in the form of LIP).
Źródło:
Acta Biochimica Polonica; 2003, 50, 1; 211-215
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
The level of endogenous DNA damage in lymphocytes isolated from blood is associated with the fluctuation of 17β-estradiol concentration in the follicular phase of healthy young women.
Autorzy:
Kapiszewska, Maria
Kalemba, Malgorzata
Grzesiak, Aneta
Kocemba, Kinga
Powiązania:
https://bibliotekanauki.pl/articles/1041444.pdf
Data publikacji:
2005
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
endogenous DNA damage
catechol-O-methyltransferase (COMT)
comet assay
17β-estradiol
Opis:
The aim of this study was to evaluate whether the differences in plasma 17β-estradiol concentration in early and late follicular phases of the menstrual cycle can affect the level of endogenous DNA damage in lymphocytes assessed by comet assay, and whether the extent of this damage in the follicular phase is associated with the genotype of catechol-O-methyltransferase (COMT). The level of DNA damage was positively correlated with 17β-estradiol concentration only in the late follicular phase. Subjects with the COMT L/L homozygous mutated variant revealed more DNA damage as compared to individuals with the COMT wild-type and heterozygous (H/L+HH) genotype.
Źródło:
Acta Biochimica Polonica; 2005, 52, 2; 535-539
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
DNA double-strand break rejoining in radioadapted human lymphocytes: evaluation by neutral comet assay and pulse-field gel electrophoresis
Autorzy:
Wojewódzka, M.
Buraczewska, I.
Szumiel, I.
Grądzka, I.
Powiązania:
https://bibliotekanauki.pl/articles/146153.pdf
Data publikacji:
2006
Wydawca:
Instytut Chemii i Techniki Jądrowej
Tematy:
human lymphocytes
radioadaptation
DNA double-strand break rejoining
neutral comet assay
pulsefield gel electrophoresis
Opis:
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.
Źródło:
Nukleonika; 2006, 51, 4; 185-191
0029-5922
1508-5791
Pojawia się w:
Nukleonika
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Effects of an antimutagen of 1,4-dihydropyridine series on cell survival and DNA damage in L5178Y murine sublines
Autorzy:
Dalivelya, O.
Savina, N.
Kuzhir, T.
Buraczewska, I.
Wojewódzka, M.
Szumiel, I.
Powiązania:
https://bibliotekanauki.pl/articles/146264.pdf
Data publikacji:
2006
Wydawca:
Instytut Chemii i Techniki Jądrowej
Tematy:
1,4-dihydropyridine
DNA repair
neutral comet assay
L5178Y cells
cytotoxicity
radioprotective effect
Opis:
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.
Źródło:
Nukleonika; 2006, 51, 3; 141-146
0029-5922
1508-5791
Pojawia się w:
Nukleonika
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Evaluation of DNA damage in white blood cells of healthy human volunteers using the alkaline comet assay and the chromosome aberration test
Autorzy:
Kopjar, Nevenka
Želježić, Davor
Garaj-Vrhovac, Verica
Powiązania:
https://bibliotekanauki.pl/articles/1041246.pdf
Data publikacji:
2006
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
peripheral blood
chromosome aberration test
white blood cells
DNA damage
alkaline comet assay
lymphocytes
Opis:
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.
Źródło:
Acta Biochimica Polonica; 2006, 53, 2; 321-336
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Evaluation of HI-6 oxime: potential use in protection of human acetylcholinesterase inhibited by antineoplastic drug irinotecan and its cyto/genotoxicity in vitro
Autorzy:
Radić, Božica
Vrdoljak, Ana
Želježić, Davor
Fuchs, Nino
Berend, Suzana
Kopjar, Nevenka
Powiązania:
https://bibliotekanauki.pl/articles/1041045.pdf
Data publikacji:
2007
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
irinotecan
HI-6
protection
reactivation
micronuclei
apoptosis
comet assay
acetylcholinesterase
chromosome aberrations
Opis:
The function of acetylcholinesterase (AChE) is the rapid hydrolysis of the neurotransmitter acetylcholine (ACh), which is involved in the numerous cholinergic pathways in both the central and the peripheral nervous system. Therefore, AChE measurement is of high value for therapy management, especially during the course of intoxication with different chemicals or drugs that inhibit the enzyme. Pyridinium or bispyridinium aldoximes (oximes) are able to recover the activity of the inhibited enzyme. Since their adverse effects are not well elucidated, in this study the efficiency of HI-6 oxime in protection and/or reactivation of human erythrocyte AChE inhibited by the antineoplastic drug irinotecan as well as its cyto/genotoxicity in vitro were investigated. HI-6 was effective in protection of AChE and increased its activity up to 30%; the residual activity after irinotecan inhibition was 7%. Also, it reactivated the enzyme previously inhibited by 50% irinotecan (4.6 µg/ml) applied at ¼ of the IC50 value. The tested concentrations of HI-6 exhibited acceptable genotoxicity towards white blood cells, as estimated by the alkaline comet assay, DNA diffusion assay and cytogenetic endpoints (structural chromosome aberrations and cytokinesis-block micronucleus assay). The results obtained warrant the further investigation of HI-6 in vivo, as well as its development for possible application in chemotherapy.
Źródło:
Acta Biochimica Polonica; 2007, 54, 3; 583-593
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Wyświetlanie 1-15 z 41

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