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    Wyświetlanie 1-4 z 4
    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:
    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:
    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:
    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
      Wyświetlanie 1-4 z 4

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