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    Wyświetlanie 1-5 z 5
    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:
    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:
    DNA damage and alterations of gene expression in chronic-degenerative diseases.
    Autorzy:
    Izzotti, Alberto
    Powiązania:
    https://bibliotekanauki.pl/articles/1043658.pdf
    Data publikacji:
    2003
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    multigene expression analysis
    DNA adducts
    human trabecular meshwork
    light
    cigarette smoke
    UV
    glaucoma
    cDNA array
    Opis:
    Chronic-degenerative diseases (CDD) recognise a variety of exogenous and endogenous risk factors interacting with the organism for many years before disease onset. We applied genomic and postgenomic molecular analyses in experimental models characterised by different contribution of exogenous and endogenous CDD risk factors. Exposure of mice to halogen light for 28 days resulted in induction of cyclobutane dimers and oxidative DNA damage in the skin. Evaluation of postgenomic alterations by cDNA arrays revealed upregulation of DNA repair pathways, increased cell division rate and protooncogenes transcription, resulting in skin tumors, 1 year later. Exposure of p53-/+ mutant mice to cigarette smoke (CS) for 28 days induced DNA adducts formation in the lung. Postgenomic alterations included decreased apoptosis and increased cell division, as compared to CS-exposed wild type mice. These phenomena resulted in lung tumors, 9 months later. Transplacental exposure of mouse foetuses to cigarette smoke induced DNA adduct formation in the liver. cDNA arrays analyses demonstrated decreased cell division, apoptosis increase, and tissue hypoxia. These phenomena resulted in growth retardation of the whole organism. Molecular alterations were investigated in human trabecular meshwork, the non-replicating ocular epithelia involved in the pathogenesis of chronic degenerative glaucoma. Results indicate increased oxidative DNA damage in glaucoma patients as compared to unaffected controls. These four experimental studies suggest that DNA damage may result in different CDD (cancer, growth retardation, glaucoma) depending on the replication rate of the target cell population.
    Źródło:
    Acta Biochimica Polonica; 2003, 50, 1; 145-154
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    High levels of bulky DNA adducts in human sperm correlate with impaired fertility.
    Autorzy:
    Horak, Stanisław
    Polańska, Joanna
    Widłak, Piotr
    Powiązania:
    https://bibliotekanauki.pl/articles/1043666.pdf
    Data publikacji:
    2003
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    fertility
    spermatozoa
    human
    DNA damage
    adducts
    32P-postlabelling
    Opis:
    Progressive decline in fertility and sperm quality has been reported over the last few decades, especially in industrialized nations. It has been proposed that exposure to factors that induce damage in DNA of spermatogenic cells may significantly contribute to impaired fertility. Here, the 32P-postlabelling method was used to analyze the levels of bulky DNA adducts in sperm cells in a group of 179 volunteers, either healthy subjects or patients with an impaired fertility. The levels of DNA adducts were 1.35-fold higher in the infertile group as compared to healthy individuals (P = 0.012). Similarly, a significant negative correlation between the levels of DNA adducts and measures of semen quality (sperm concentration and motility) has been observed (P Ł 0.001). In addition, the levels of bulky DNA adducts in sperm cells positively correlates with amounts of leukocytes in semen, which were significantly higher in semen of infertile subjects.
    Źródło:
    Acta Biochimica Polonica; 2003, 50, 1; 197-203
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Mismatch dependent uracil/thymine-DNA glycosylases excise exocyclic hydroxyethano and hydroxypropano cytosine adducts.
    Autorzy:
    Borys-Brzywczy, Ewa
    Arczewska, Katarzyna
    Saparbaev, Murat
    Hardeland, Ulrike
    Schär, Primo
    Kuśmierek, Jarosław
    Powiązania:
    https://bibliotekanauki.pl/articles/1041473.pdf
    Data publikacji:
    2005
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    base excision repair
    E. coli mismatch uracil-DNA glycosylase
    exocyclic cytosine adducts
    human thymine-DNA glycosylase
    S. pombe Thp1p glycosylase
    Opis:
    Exocyclic adducts of DNA bases, such as etheno- and hydroxyalkano- ones, are generated by a variety of bifunctional agents, including endogenously formed products of lipid peroxidation. In this work we selectively modified cytosines in the 5'-d(TTT TTT CTT TTT CTT TTT CTT TTT T)-3' oligonucleotide using: chloroacetaldehyde to obtain 3,N4-α-hydroxyethano- (HEC) and 3,N4-etheno- (εC), acrolein to obtain 3,N4-α-hydroxypropano- (HPC) and crotonaldehyde to obtain 3,N4-α-hydroxy-γ-methylpropano- (mHPC) adducts of cytosine. The studied adducts are alkali-labile which results in oligonucleotide strain breaks at the sites of modification upon strong base treatment. The oligonucleotides carrying adducted cytosines were studied as substrates of Escherichia coli Mug, human TDG and fission yeast Thp1p glycosylases. All the adducts studied are excised by bacterial Mug although with various efficiency: εC >HEC >HPC >mHPC. The yeast enzyme excises efficiently εC ł HEC >HPC, whereas the human enzyme excises only εC. The pH-dependence curves of excision of εC, HEC and HPC by Mug are bell shaped and the most efficient excision of adducts occurs within the pH range of 8.6-9.6. The observed increase of excision of HEC and HPC above pH 7.2 can be explained by deprotonation of these adducts, which are high pKa compounds and exist in a protonated form at neutrality. On the other hand, since εC is in a neutral form in the pH range studied, we postulate an involvement of an additional catalytic factor. We hypothesize that the enzyme structure undergoes a pH-induced rearrangement allowing the participation of Lys68 of Mug in catalysis via a hydrogen bond interaction of its ε-amino group with N4 of the cytosine exocyclic adducts.
    Źródło:
    Acta Biochimica Polonica; 2005, 52, 1; 149-165
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
      Wyświetlanie 1-5 z 5

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