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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:
Sirt3 regulates the level of mitochondrial DNA repair activity through deacetylation of NEIL1, NEIL2, OGG1, MUTYH, APE1 and LIG3 in colorectal cancer
Autorzy:
Kabziński, Jacek
Walczak, Anna
Mik, Michał
Majsterek, Ireneusz
Powiązania:
https://bibliotekanauki.pl/articles/1391859.pdf
Data publikacji:
2020
Wydawca:
Index Copernicus International
Tematy:
cancer
colorectal cancer
DNA damage/repair
genetics
proteins
Opis:
Colorectal cancer (CRC) is one of the most common malignant tumors. One of the factors increasing the risk of its occurrence may be the reduced efficiency of repairing DNA damage, both nuclear and mitochondrial. The main mechanism for repairing oxidative damage is the BER system (in mitochondria mtBER), whose key proteins NEIL1, NEIL2, OGG1, MUTYH, APE1 and LIG3 obtain full efficiency only at the appropriate level of acetylation. Sirtuin 3 is a key protein for mitochondrial homeostasis, regulating a number of metabolic processes related mainly to the control of the level of reactive oxygen species. Because Sirt3 possesses acetylase activity, it can modulate the level of activity of mtBER proteins by their deacetylation. The conducted study showed that the tested proteins NEIL1, NEIL2, OGG1, MUTYH, APE1 and LIG3 are the substrate for the enzymatic deacetylation activity of Sirt3, which may lead to modulation of the risk of CRC, and in cancer cells may be a potential therapeutic target enhancing the action of cytostatic drugs.
Źródło:
Polish Journal of Surgery; 2020, 92, 1; 1-4
0032-373X
2299-2847
Pojawia się w:
Polish Journal of Surgery
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Sequence-specific p53 gene damage by chloroacetaldehyde and its repair kinetics in Escherichia coli
Autorzy:
Kowalczyk, Paweł
Cieśla, Jarosław
Saparbaev, Murat
Laval, Jacques
Tudek, Barbara
Powiązania:
https://bibliotekanauki.pl/articles/1041247.pdf
Data publikacji:
2006
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
chloroacetaldehyde
p53
replication
exocyclic DNA adducts
vinyl chloride
LM-PCR
DNA repair
sequence-specific DNA damage
Opis:
Oxidative stress and certain environmental carcinogens, e.g. vinyl chloride and its metabolite chloroacetaldehyde (CAA), introduce promutagenic exocyclic adducts into DNA, among them 1,N6-ethenoadenine (εA), 3,N4-ethenocytosine (εC) and N2,3-ethenoguanine (εG). We studied sequence-specific interaction of the vinyl-chloride metabolite CAA with human p53 gene exons 5-8, using DNA Polymerase Fingerprint Analysis (DPFA), and identified sites of the highest sensitivity. CAA-induced DNA damage was more extensive in p53 regions which revealed secondary structure perturbations, and were localized in regions of mutation hot-spots. These perturbations inhibited DNA synthesis on undamaged template. We also studied the repair kinetics of CAA-induced DNA lesions in E. coli at nucleotide resolution level. A plasmid bearing full length cDNA of human p53 gene was modified in vitro with 360 mM CAA and transformed into E. coli DH5α strain, in which the adaptive response system had been induced by MMS treatment before the cells were made competent. Following transformation, plasmids were re-isolated from transformed cultures 35, 40, 50 min and 1-24 h after transformation, and further subjected to LM-PCR, using ANPG, MUG and Fpg glycosylases to identify the sites of DNA damage. In adaptive response-induced E. coli cells the majority of DNA lesions recognized by ANPG glycosylase were removed from plasmid DNA within 35 min, while MUG glycosylase excised base modifications only within 50 min, both in a sequence-dependent manner. In non-adapted cells resolution of plasmid topological forms was perturbed, suggesting inhibition of one or more bacterial topoisomerases by unrepaired ε-adducts. We also observed delayed consequences of DNA modification with CAA, manifesting as secondary DNA breaks, which appeared 3 h after transformation of damaged DNA into E. coli, and were repaired after 24 h.
Źródło:
Acta Biochimica Polonica; 2006, 53, 2; 337-347
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Repair of γ-ray-induced base damage in L5178Y sublines is damage type-dependent and unrelated to radiation sensitivity.
Autorzy:
Kruszewski, Marcin
Zastawny, Tomasz
Szumiel, Irena
Powiązania:
https://bibliotekanauki.pl/articles/1044148.pdf
Data publikacji:
2001
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
radiation sensitivity
: γ-rays
DNA base damage repair
L5178Y murine lymphoma sublines
Opis:
The L5178Y (LY) murine lymphoma sublines LY-R and LY-S are differentially sensitive to ionizing radiation. The high radiation sensitivity of LY-S cells is related to impaired rejoining of DNA double strand breaks. We found previously that the γ-ray-induced base damage is higher in the more radiosensitive LY-S subline. Here, we examine the role of the repair of ionizing radiation induced base damage in relation to the radiosensitivity difference of these sublines. We used the GS/MS technique to estimate the repair rates of six types of base damage in γ-irradiated LY cells. All modified DNA bases identified in the course of this study were typical for irradiated chromatin. The total amount of initial base damage was higher in the radiation sensitive LY-S subline than in the radiation resistant LY-R subline. The repair rates of 5-OHMeUra, 5-OHCyt, 8-OHAde were similar in both cell lines, the repair rates of FapyAde and 8-OHGua were higher in the radiosensitive LY-S cell line, whereas the repair of 5-OHUra was faster in its radioresistant counterpart, the LY-R Altogether, the repair rates of the γ-ray-induced DNA base damage in LY sublines are related neither to the initial amounts of the damaged bases nor to the differential lethal or mutagenic effects of ionizing radiation in these sublines.
Źródło:
Acta Biochimica Polonica; 2001, 48, 2; 525-533
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Recognition and repair of DNA-cisplatin adducts.
Autorzy:
Woźniak, Katarzyna
Błasiak, Janusz
Powiązania:
https://bibliotekanauki.pl/articles/1043720.pdf
Data publikacji:
2002
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
DNA-protein crosslinks
cisplatin
DNA adducts
DNA damage
DNA repair
cis-diamminedichloroplatinum
Opis:
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.
Źródło:
Acta Biochimica Polonica; 2002, 49, 3; 583-596
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Reactive oxygen species in BCR-ABL1-expressing cells - relevance to chronic myeloid leukemia
Autorzy:
Antoszewska-Smith, Joanna
Pawlowska, Elzbieta
Blasiak, Janusz
Powiązania:
https://bibliotekanauki.pl/articles/1038675.pdf
Data publikacji:
2017
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
chronic myeloid leukemia
reactive oxygen species
DNA damage
DNA repair
cancer stem cells
imatinib resistance
Opis:
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.
Źródło:
Acta Biochimica Polonica; 2017, 64, 1; 1-10
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:
Polimorfizm genów kodujących białka naprawy DNA a zawodowe i środowiskowe narażenie na ołów, arsen i pestycydy
Polymorphism of genes encoding proteins of DNA repair vs. occupational and environmental exposure to lead, arsenic and pesticides
Autorzy:
Bukowski, Karol
Woźniak, Katarzyna
Powiązania:
https://bibliotekanauki.pl/articles/2162666.pdf
Data publikacji:
2018-03-09
Wydawca:
Instytut Medycyny Pracy im. prof. dra Jerzego Nofera w Łodzi
Tematy:
polimorfizm genetyczny
arsen
pestycydy
ołów
uszkodzenia DNA
geny naprawy DNA
genetic polymorphism
arsenic
pesticides
lead
DNA damage
DNA repair genes
Opis:
Polimorfizm genetyczny wiąże się z występowaniem w populacji co najmniej 2 różnych alleli w danym locus z częstością większą niż 1%. Wyróżniamy m.in. polimorfizm pojedynczego nukleotydu (single nucleotide polymorphism – SNP) i polimorfizm zmiennej liczby powtórzeń tandemowych. Występowanie określonych polimorfizmów w genach kodujących enzymy naprawy DNA jest związane z szybkością i wydajnością naprawy DNA oraz może chronić lub narażać daną osobę na skutki działania określonego ksenobiotyku. Związki chemiczne takie, jak ołów, arsen i pestycydy odznaczają się dużą toksycznością. Opisano wiele różnych polimorfizmów genów kodujących enzymy naprawy DNA, które mają wpływ na skuteczność naprawy uszkodzeń DNA indukowanych przez te ksenobiotyki. W przypadku ołowiu zbadano wpływ polimorfizmów genów: APE1 (apurinic/apyrimidinic endonuclease 1 – endonukleaza miejsca apurynowego/apirymidynowego) (rs1130409), hOGG1 (human 8-oxoguanine glycosylase – glikozylaza 8-oksyguaniny) (rs1052133), XRCC1 (X-ray repair cross-complementing protein group 1 – białko biorące udział w naprawie DNA przez wycinanie zasad) (rs25487), XRCC1 (rs1799782) oraz XRCC3 (X-ray repair cross-complementing protein group 3 – białko biorące udział w naprawie DNA przez rekombinację homologiczną) (rs861539). Dla arsenu przedstawiono w niniejszej pracy wyniki badań dotyczących następujących polimorfizmów: ERCC2 (excision repair cross-complementing – białko biorące udział w naprawie DNA przez wycinanie nukleotydów) (rs13181), XRCC3 (rs861539), APE1 (rs1130409) oraz hOGG1 (rs1052133). W odniesieniu do pestycydów w pracy przedstawiono zarówno osobny, jak i łączny wpływ polimorfizmów genów takich, jak XRCC1 (rs1799782), hOGG1 (rs1052133), XRCC4 (X-ray repair cross-complementing protein group 4 – białko biorące udział w naprawie DNA przez łączenie końców niehomologicznych) (rs28360135) i genu kodującego enzym detoksykacyjny paraoksonazę PON1 (paraoxonase 1) (rs662). Med. Pr. 2018;69(2):225–235
Genetic polymorphism is associated with the occurrence of at least 2 different alleles in the locus with a frequency higher than 1% in the population. Among polymorphisms we can find single nucleotide polymorphism (SNP) and polymorphism of variable number of tandem repeats. The presence of certain polymorphisms in genes encoding DNA repair enzymes is associated with the speed and efficiency of DNA repair and can protect or expose humans to the effects provoked by xenobiotics. Chemicals, such as lead, arsenic pesticides are considered to exhibit strong toxicity. There are many different polymorphisms in genes encoding DNA repair enzymes, which determine the speed and efficiency of DNA damage repair induced by these xenobiotics. In the case of lead, the influence of various polymorphisms, such as APE1 (apurinic/apyrimidinic endonuclease 1) (rs1130409), hOGG1 (human 8-oxoguanine glycosylase) (rs1052133), XRCC1 (X-ray repair cross-complementing protein group 1) (rs25487), XRCC1 (rs1799782) and XRCC3 (X-ray repair cross-complementing protein group 3) (rs861539) were described. For arsenic polymorphisms, such as ERCC2 (excision repair cross-complementing) (rs13181), XRCC3 (rs861539), APE1 (rs1130409) and hOGG1 (rs1052133) were examined. As to pesticides, separate and combined effects of polymorphisms in genes encoding DNA repair enzymes, such as XRCC1 (rs1799782), hOGG1 (rs1052133), XRCC4 (X-ray repair cross-complementing protein group 4) (rs28360135) and the gene encoding the detoxification enzyme PON1 paraoxonase (rs662) were reported. Med Pr 2018;69(2):225–235
Źródło:
Medycyna Pracy; 2018, 69, 2; 225-235
0465-5893
2353-1339
Pojawia się w:
Medycyna Pracy
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Oksydacyjne uszkodzenia DNA w chorobie Alzheimera i Creutzfeldta-Jakoba
DNA oxidative damage in Alzheimer’s and Creutzfeldt-Jakob disease
Autorzy:
Grešner, Sylwia M.
Liberski, Paweł P.
Powiązania:
https://bibliotekanauki.pl/articles/1057838.pdf
Data publikacji:
2011
Wydawca:
Medical Communications
Tematy:
Alzheimer’s disease
Creutzfeldt-Jakob disease
DNA damage
DNA repair genes
oxidative stress
stres oksydacyjny
choroba Creutzfeldta-Jakoba
geny naprawy DNA
uszkodzenia DNA
choroba Alzhaimera
Opis:
The loss of nerve cells and the accumulation of pathological protein deposits comprise the common features of Alzheimer’s disease (AD) and Creutzfeldt-Jakob disease (CJD). Despite our constantly broadening knowledge of the pathogenesis of neurodegenerative diseases, the precise molecular mechanisms of the pathological processes underlying this group of diseases still remain to be unambiguously elucidated. Recently, evidence suggesting a crucial role for the oxidation stress in the development of these neurodegenerative diseases has significantly increased. An association between the accumulation of pathological protein deposits and increased generation of reactive oxygen species has been proposed in both AD and CJD. In the light of increasing evidence documenting the occurrence of DNA damage as a consequence of oxidative stress, involvement of DNA repair genes in the pathogenesis of these diseases was implicated. The product of OGG1, APE1 and XRCC1 genes play various roles in the removal of oxidative-stress-induced DNA damage, and in the protection of cells against the consequences of oxidative stress, including cell death. The enzymes comprising the DNA repair system play a significant role in maintaining an intact genome. Therefore, the dysfunction of this system or its partial impairment may lead to an accumulation of errors which ultimately lead to cell death.
Wspólną cechą choroby Alzheimera (AD) i Creutzfeldta-Jakoba (CJD) jest utrata komórek nerwowych oraz gromadzenie się w mózgu złogów nieprawidłowo zwiniętych białek. Pomimo coraz szerszej wiedzy na temat patogenezy chorób neurodegeneracyjnych precyzyjne mechanizmy molekularne procesów patologicznych w tej grupie chorób wciąż nie zostały jednoznacznie wyjaśnione. W ostatnich latach wzrosła liczba dowodów na to, że stres oksydacyjny odgrywa ważną rolę w rozwoju tych chorób neurodegeneracyjnych. Proponuje się związek pomiędzy odkładaniem nieprawidłowych form białek a wzrostem produkcji reaktywnych form tlenu, zarówno w przypadku AD, jak i CJD. W świetle licznych dowodów występowania uszkodzeń DNA wywołanych działaniem stresu oksydacyjnego postuluje się zaangażowanie genów naprawy DNA w patogenezę tych chorób. Produkty genów naprawy OGG1, APE1, XRCC1 są zaangażowane w usuwanie oksydacyjnych uszkodzeń DNA i ochronę komórki przed zgubnymi skutkami stresu oksydacyjnego, włącznie ze śmiercią komórkową. Enzymy systemu naprawy uszkodzeń DNA odgrywają istotną rolę w utrzymaniu integracji genomu. W przypadku ich całkowitego braku lub uszkodzeń w komórkach dochodzi do gromadzenia błędów, które prowadzą do śmierci komórki.
Źródło:
Aktualności Neurologiczne; 2011, 11, 1; 64-67
1641-9227
2451-0696
Pojawia się w:
Aktualności Neurologiczne
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Impact of the Ser326Cys polymorphism of the OGG1 gene on the level of oxidative DNA damage in patients with colorectal cancer
Autorzy:
Kabzinski, Jacek
Walczak, Anna
Dziki, Adam
Mik, Michał
Majsterek, Ireneusz
Powiązania:
https://bibliotekanauki.pl/articles/1392877.pdf
Data publikacji:
2018
Wydawca:
Index Copernicus International
Tematy:
colorectal cancer
OGG1
8-oxoguanine
DNA repair
oxidative damage
Opis:
As a result of reactive oxygen species operation, cell damage occurs in both cellular organelles and molecules, including DNA. Oxidative damage within the genetic material can lead to accumulation of mutations and consequently to cancer transformation. OGG1 glycosylase, a component of the Base Excision Repair (BER) system, is one of the enzymes that prevents excessive accumulation of 8-oxoguanine (8-oxG), the most common compound formed by oxidative DNA damage. In case of structural changes of OGG1 resulting from polymorphic variants, we can observe a significant increase in the concentration of 8-oxG. Linking individual polymorphisms to DNA repair systems with increased risk of colorectal cancer will allow patients to be classified as high risk and included in a prophylactic program. The aim of the study was to determine the level of oxidative DNA damage and to analyze the distribution of Ser326Cys polymorphism of the OGG1 gene in a group of patients with colorectal cancer and in a control group in the Polish population. Material and methodology. DNA was isolated from the blood of 174 patients with colorectal cancer. The control group consisted of 176 healthy individuals. The level of oxidative damage was determined by analyzing the amount of 8-oxguanine using the HT 8-oxo-dG ELISA II Kit. Genotyping was performed via the TaqMan method. Results. The obtained results indicate that Ser326Cys polymorphism of the OGG1 gene increases the risk of RJG and is associated with significantly increased levels of 8-oxoguanine. Conclusions. Based on the results obtained, we conclude that Ser326Cys polymorphism of the OGG1 gene may modulate the risk of colorectal cancer by increasing the level of oxidative DNA damage.
Źródło:
Polish Journal of Surgery; 2018, 90, 2; 13-15
0032-373X
2299-2847
Pojawia się w:
Polish Journal of Surgery
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:
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:
Detection of damage-recognition proteins from human lymphocytes.
Autorzy:
Łanuszewska, Joanna
Cudak, Anna
Rzeszowska-Wolny, Joanna
Widłak, Piotr
Powiązania:
https://bibliotekanauki.pl/articles/1044373.pdf
Data publikacji:
2000
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
damage recognition
human lymphocytes
damaged DNA-binding proteins
repair capacity
Opis:
Proteins recognizing and binding to damaged DNA (DDB-proteins) were analyzed in human lymphocytes obtained from healthy donors. Using an electrophoretic mobility shift assay several complexes between nuclear extract proteins and damaged DNA were detected: a complex specific for DNA damaged by N-acetoxy-N-acetylaminofluorene, another complex specific for UV-irradiated DNA, and two complexes specific for DNA damaged by cis-dichlorodiammine platinum. All the detected complexes differed in electrophoretic mobility and possibly contained different proteins. Complexes specific for free DNA ends were also detected in protein extracts from lymphocytes.
Źródło:
Acta Biochimica Polonica; 2000, 47, 2; 443-450
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Charge transfer in DNA and repair of oxidative damage
Autorzy:
Męczyńska, S.
Szumiel, I.
Powiązania:
https://bibliotekanauki.pl/articles/146454.pdf
Data publikacji:
2009
Wydawca:
Instytut Chemii i Techniki Jądrowej
Tematy:
charge transfer in DNA
DNA repair
oxidative base damage
base damage excision
4Fe-4S cluster
MutY glycosylase
photolyase
Opis:
The possibility of a biological role of an unusual function of DNA sequences is discussed, namely, signaling by charge transfer within chromatin. Although a general conclusion on its biological significance is premature, the idea of charge transfer accompanying repair of some types of oxidative DNA damage is based on sound experimental data. Both physical and chemical experiments reviewed here provided results indicating that DNA duplex under certain conditions (among them – hydration) – can behave as narrow band gap semiconductor. With the use of model molecules it was shown that charge transfer most probably occurs by hopping between guanine residues and tunneling through thymine-adenine (TA) base pairs. Charge transfer is nucleotide sequence and distance dependent. Furthermore, the pi-stacked base pairs must be perfectly matched to mediate charge transfer and in a damaged double helix this condition is not fulfilled. Hence, the possibility that charge transfer takes place in oxidatively damaged DNA after UV or X-irradiation and it becomes interrupted by mismatched base pairs, thus signaling the mismatch or strand break to the repair machinery. Function of base damage repair enzymes which contain [4Fe-4S] clusters is discussed in this context.
Źródło:
Nukleonika; 2009, 54, 1; 11-16
0029-5922
1508-5791
Pojawia się w:
Nukleonika
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Bacterial DNA repair genes and their eukaryotic homologues: 4. The role of nucleotide excision DNA repair (NER) system in mammalian cells
Autorzy:
Maddukuri, Leena
Dudzińska, Dominika
Tudek, Barbara
Powiązania:
https://bibliotekanauki.pl/articles/1040922.pdf
Data publikacji:
2007
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
trichothiodystrophy
Cockayne syndrome
xeroderma pigmentosum
DNA damage
DNA repair
nucleotide excision repair
Opis:
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).
Źródło:
Acta Biochimica Polonica; 2007, 54, 3; 469-482
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
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