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Wyszukujesz frazę "DNA oxidative damage repair" wg kryterium: Temat

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    Wyświetlanie 1-6 z 6
    Tytuł:
    Antioxidant and DNA repair stimulating effect of extracts from Leonurus sibiricus against an induced oxidative stress and DNA damage in CHO cells
    Autorzy:
    Sitarek, P.
    Skala, E.
    Wysokinska, H.
    Wielanek, M.
    Szemraj, J.
    Sliwinski, T.
    Powiązania:
    https://bibliotekanauki.pl/articles/951184.pdf
    Data publikacji:
    2015
    Wydawca:
    Polska Akademia Nauk. Czytelnia Czasopism PAN
    Tematy:
    conference
    antioxidant
    DNA repair
    stimulating effect
    Leonurus sibiricus
    oxidative stress
    DNA damage
    secondary metabolite
    polyphenolic acid
    flavonoids
    Chinese hamster ovary
    Źródło:
    BioTechnologia. Journal of Biotechnology Computational Biology and Bionanotechnology; 2015, 96, 1
    0860-7796
    Pojawia się w:
    BioTechnologia. Journal of Biotechnology Computational Biology and Bionanotechnology
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Assessment of DNA damage profile and oxidative /antioxidative biomarker level in patients with inflammatory bowel disease
    Autorzy:
    Mrowicka, Małgorzata
    Mrowicki, Jerzy
    Mik, Michał
    Dziki, Łukasz
    Dziki, Adam
    Majsterek, Ireneusz
    Powiązania:
    https://bibliotekanauki.pl/articles/1391884.pdf
    Data publikacji:
    2020
    Wydawca:
    Index Copernicus International
    Tematy:
    DNA oxidative damage repair
    inflammatory bowel diseases
    pro/antioxidant status
    Opis:
    Aim: The purpose of this study was to investigate the oxidative DNA damage, pro-antioxidant status in Polish patients with inflammatory bowel disease (IBD). Methods: Oxidative DNA damage was measured by comet assay techniques; nitric oxide (NO) and plasmatic lipid peroxidation (MDA) as oxidative stress were valuated by colometric methods; superoxide dismutase (SOD1), catalase (CAT) and glutathione peroxidase (GPx1) as antioxidative defense were determined by spectrophotometric methods. Results: The level of oxidative DNA damage in IBD patients was significantly higher in relation to controls (P = 0.01). Alike, in control subject as well as in patients with IBD, lymphocytes are characterized by complete repair of DNA damage. A significant decrease of SOD (P = 0.031), CAT (P = 0.006), GPx1 (P = 0.001) activity was seen in IBD patients vs control. MDA (P = 0.001) and NO (P = 0.001) concentrations were significantly increased in IBD patients as compared to healthy subjects. Conclusions: Our results may be due to the induction of DNA repair genes which may occur at the stage of the pathological changes (IBD) that may be caused by excessive oxidative stress. However, the cause of this relationship, and whether it is direct or indirect, remains to be explored.
    Źródło:
    Polish Journal of Surgery; 2020, 92, 5; 8-14
    0032-373X
    2299-2847
    Pojawia się w:
    Polish Journal of Surgery
    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:
    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:
    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:
    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
      Wyświetlanie 1-6 z 6

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