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Tytuł:
A new look at adaptive mutations in bacteria.
Autorzy:
Janion, Celina
Powiązania:
https://bibliotekanauki.pl/articles/1044374.pdf
Data publikacji:
2000
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
adaptive mutations
DNA damage
DNA repair
Opis:
This is a short survey of the adaptive mutation processes that arise in non- or slowly- dividing bacterial cells and includes: (i) bacterial models in which adaptive mutations are studied; (ii) the mutagenic lesions from which these mutations derive; (iii) the influence of DNA repair processes on the spectrum of adaptive mutations. It is proposed that in starved cells, likely as during the MFD phenomenon, lesions in tRNA suppressor genes are preferentially repaired and no suppressor tRNAs are formed as a result of adaptive mutations. Perhaps the most provocative proposal is (iv) a hypothesis that the majority of adaptive mutations are selected in a pre-apoptotic state where the cells are either mutated, selected, and survive, or they die.
Źródło:
Acta Biochimica Polonica; 2000, 47, 2; 451-457
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Mutations in DNA polymerase gamma cause error prone DNA synthesis in human mitochondrial disorders
Autorzy:
Copeland, William
Ponamarev, Mikhail
Nguyen, Dinh
Kunkel, Thomas
Longley, Matthew
Powiązania:
https://bibliotekanauki.pl/articles/1043659.pdf
Data publikacji:
2003
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
aging
DNA replication
mitochondria
DNA repair
DNA polymerase
Opis:
This paper summarizes recent advances in understanding the links between the cell's ability to maintain integrity of its mitochondrial genome and mitochondrial genetic diseases. Human mitochondrial DNA is replicated by the two-subunit DNA polymerase γ (pol γ). We investigated the fidelity of DNA replication by pol γ with and without exonucleolytic proofreading and its p55 accessory subunit. Pol γ has high base substitution fidelity due to efficient base selection and exonucleolytic proofreading, but low frameshift fidelity when copying homopolymeric sequences longer than four nucleotides. Progressive external ophthalmoplegia (PEO) is a rare disease characterized by the accumulation of large deletions in mitochondrial DNA. Recently, several mutations in the polymerase and exonuclease domains of the human pol γ have been shown to be associated with PEO. We are analyzing the effect of these mutations on the human pol γ enzyme. In particular, three autosomal dominant mutations alter amino acids located within polymerase motif B of pol γ. These residues are highly conserved among family A DNA polymerases, which include T7 DNA polymerase and E. coli pol I. These PEO mutations have been generated in pol γ to analyze their effects on overall polymerase function as well as the effects on the fidelity of DNA synthesis. One mutation in particular, Y955C, was found in several families throughout Europe, including one Belgian family and five unrelated Italian families. The Y955C mutant pol γ retains a wild-type catalytic rate but suffers a 45-fold decrease in apparent binding affinity for the incoming dNTP. The Y955C derivative is also much less accurate than is wild-type pol γ, with error rates for certain mismatches elevated by 10- to 100-fold. The error prone DNA synthesis observed for the Y955C pol γ is consistent with the accumulation of mtDNA mutations in patients with PEO. The effects of other pol γ mutations associated with PEO are discussed.
Źródło:
Acta Biochimica Polonica; 2003, 50, 1; 155-167
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
The pH optimum of native uracil-DNA glycosylase of Archaeoglobus fulgidus compared to recombinant enzyme indicates adaption to cytosolic pH
Autorzy:
Knævelsrud, Ingeborg
Kazazic, Sabina
Birkeland, Nils-Kåre
Bjelland, Svein
Powiązania:
https://bibliotekanauki.pl/articles/1039311.pdf
Data publikacji:
2014
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
DNA repair
uracil-DNA glycosylase
uracil
deamination
hyperthermophiles
Opis:
Uracil-DNA glycosylase of Archaeoglobus fulgidus (Afung) in cell extracts exhibited maximal activity around pH 6.2 as compared to pH 4.8 for the purified recombinant enzyme expressed in Escherichia coli. Native Afung thus seems to be adapted to the intracellular pH of A. fulgidus, determined to be 7.0±0.1. Both recombinant and native Afung exhibited a broad temperature optimum for activity around 80°C, reflecting the A. fulgidus optimal growth temperature of 83°C. Adaption to the neutral conditions in the A. fulgidus cytoplasm might be due to covalent modifications or accessory factors, or due to a different folding when expressed in the native host.
Źródło:
Acta Biochimica Polonica; 2014, 61, 2; 393-395
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Bacterial DNA repair genes and their eukaryotic homologues: 3. AlkB dioxygenase and Ada methyltransferase in the direct repair of alkylated DNA
Autorzy:
Nieminuszczy, Jadwiga
Grzesiuk, Elżbieta
Powiązania:
https://bibliotekanauki.pl/articles/1040921.pdf
Data publikacji:
2007
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
alkylating agents
adaptive response
AlkB
DNA repair
Opis:
Environmental and endogenous alkylating agents generate cytotoxic and mutagenic lesions in DNA. Exposure of prokaryotic cells to sublethal doses of DNA alkylating agents induces so called adaptive response (Ada response) involving the expression of a set of genes which allows the cells to tolerate the toxic and mutagenic action of such agents. The Ada response includes the expression of four genes: ada, alkA, alkB, and aidB. The product of ada gene, Ada protein, is an activator of transcription of all four genes. DNA bases damaged by alkylation are removed by distinct strategies. The most toxic lesion 3meA is removed by specific DNA glycosylase initiating base excising repair. The toxic and mutagenic O6meG is repaired directly by methyltransferases. 1meA and 3meC are corrected by AlkB DNA dioxygenase. The mechanisms of action of E. coli AlkB dioxygenase and its human homologs ABH2 and ABH3 are described in more details.
Źródło:
Acta Biochimica Polonica; 2007, 54, 3; 459-468
0001-527X
Pojawia się w:
Acta Biochimica Polonica
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
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:
Hyperthermia can differentially modulate the repair of doxorubicin-damaged DNA in normal and cancer cells*.
Autorzy:
Blasiak, Janusz
Widera, Kinga
Pertyński, Tomasz
Powiązania:
https://bibliotekanauki.pl/articles/1043663.pdf
Data publikacji:
2003
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
hyperthermia
drug resistance
K562 cells
DNA repair
Opis:
Hyperthermia can modulate the action of many anticancer drugs, and DNA repair processes are temperature-dependent, but the character of this dependence in cancer and normal cells is largely unknown. This subject seems to be worth studying, because hyperthermia can assist cancer therapy. A 1-h incubation at 37°C of normal human peripheral blood lymphocytes and human myelogenous leukemia cell line K562 with 0.5 μM doxorubicin gave significant level of DNA damage as assessed by the alkaline comet assay. The cells were then incubated in doxorubicin-free repair medium at 37°C or 41°C. The lymphocytes incubated at 37°C needed about 60 min to remove completely the damage to their DNA, whereas at 41°C the time required for complete repair was shortened to 30 min. There was also a difference between the repair kinetics at 37°C and 41°C in cancer cells. Moreover, the kinetics were different in doxorubicin-sensitive and resistant cells. Therefore, hyperthermia may significantly affect the kinetics of DNA repair in drug-treated cells, but the magnitude of the effect may be different in normal and cancer cells. These features may be exploited in cancer chemotherapy to increase the effectiveness of the treatment and reduce unwanted effects of anticancer drugs in normal cells and fight DNA repair-based drug resistance of cancer cells.
Źródło:
Acta Biochimica Polonica; 2003, 50, 1; 191-195
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Bacterial DNA repair genes and their eukaryotic homologues: 5. The role of recombination in DNA repair and genome stability
Autorzy:
Nowosielska, Anetta
Powiązania:
https://bibliotekanauki.pl/articles/1040931.pdf
Data publikacji:
2007
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
homologous recombination
Escherichia coli
DSB
replication forks
DNA repair
Opis:
Recombinational repair is a well conserved DNA repair mechanism present in all living organisms. Repair by homologous recombination is generally accurate as it uses undamaged homologous DNA molecule as a repair template. In Escherichia coli homologous recombination repairs both the double-strand breaks and single-strand gaps in DNA. DNA double-strand breaks (DSB) can be induced upon exposure to exogenous sources such as ionizing radiation or endogenous DNA-damaging agents including reactive oxygen species (ROS) as well as during natural biological processes like conjugation. However, the bulk of double strand breaks are formed during replication fork collapse encountering an unrepaired single strand gap in DNA. Under such circumstances DNA replication on the damaged template can be resumed only if supported by homologous recombination. This functional cooperation of homologous recombination with replication machinery enables successful completion of genome duplication and faithful transmission of genetic material to a daughter cell. In eukaryotes, homologous recombination is also involved in essential biological processes such as preservation of genome integrity, DNA damage checkpoint activation, DNA damage repair, DNA replication, mating type switching, transposition, immune system development and meiosis. When unregulated, recombination can lead to genome instability and carcinogenesis.
Źródło:
Acta Biochimica Polonica; 2007, 54, 3; 483-494
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:
Inhibition of DNA repair glycosylases by base analogs and tryptophan pyrolysate, Trp-P-1.
Autorzy:
Speina, Elżbieta
Cieśla, Jarosław
Grąziewicz, Maria-Anna
Laval, Jacques
Kazimierczuk, Zygmunt
Tudek, Barbara
Powiązania:
https://bibliotekanauki.pl/articles/1041475.pdf
Data publikacji:
2005
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
base analogs
Trp-P-1
DNA repair enzymes
inhibitors
formamidopyrimidine DNA glycosylase
Opis:
DNA base analogs, 2,4,5,6-substituted pyrimidines and 2,6-substituted purines were tested as potential inhibitors of E. coli Fpg protein (formamidopyrimidine -DNA glycosylase). Three of the seventeen compounds tested revealed inhibitory properties. 2-Thioxanthine was the most efficient, inhibiting 50% of 2,6-diamino-4-hydroxy-5N-methyl-formamidopyrimidine (Fapy-7MeG) excision activity at 17.1 μM concentration. The measured Kgi was 4.44 ± 0.15 μM. Inhibition was observed only when the Fpg protein was first challenged to its substrate followed by the addition of the base analog, suggesting uncompetitive (catalytic) inhibition. For two other compounds, 2-thio- or 2-oxo-4,5,6-substituted pyrimidines, IC50 was only 343.3 ± 58.6 and 350 ± 24.4 μM, respectively. No change of the Fpg glycosylase activity was detected in the presence of Fapy-7MeG, up to 5 μM. We also investigated the effect of DNA structure modified by tryptophan pyrolysate (Trp-P-1) on the activity of base excision repair enzymes: Escherichia coli and human DNA glycosylases of oxidized (Fpg, Nth) and alkylated bases (TagA, AlkA, and ANPG), and for bacterial AP endonuclease (Xth protein). Trp-P-1, which changes the secondary DNA structure into non-B, non-Z most efficiently inhibited excision of alkylated bases by the AlkA glycosylase (IC50 = 1 μM). The ANPG, TagA, and Fpg proteins were also inhibited although to a lesser extent (IC50 = 76.5 μM, 96 μM, and 187.5 μM, respectively). Trp-P-1 also inhibited incision of DNA at abasic sites by the β-lyase activity of the Fpg and Nth proteins, and to a lesser extent by the Xth AP endonuclease. Thus, DNA conformation is critical for excision of damaged bases and incision of abasic sites by DNA repair enzymes.
Źródło:
Acta Biochimica Polonica; 2005, 52, 1; 167-178
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Poly(ADP-ribose) polymerase in base excision repair: always engaged, but not essential for DNA damage processing.
Autorzy:
Allinson, Sarah
Dianova, Irina
Dianov, Grigory
Powiązania:
https://bibliotekanauki.pl/articles/1043660.pdf
Data publikacji:
2003
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
PARP
base excision repair
cell extracts
in vitro repair
abasic sites
DNA repair
Opis:
Poly(ADP-ribose) polymerase (PARP-1) is an abundant nuclear protein with a high affinity for single- and double-strand DNA breaks. Its binding to strand breaks promotes catalysis of the covalent modification of nuclear proteins with poly(ADP-ribose) synthesised from NAD+. PARP-1-knockout cells are extremely sensitive to alkylating agents, suggesting the involvement of PARP-1 in base excision repair; however, its role remains unclear. We investigated the dependence of base excision repair pathways on PARP-1 and NAD+ using whole cell extracts derived from normal and PARP-1 deficient mouse cells and DNA substrates containing abasic sites. In normal extracts the rate of repair was highly dependent on NAD+. We found that in the absence of NAD+ repair was slowed down 4-6-fold after incision of the abasic site. We also established that in extracts from PARP-1 deficient mouse cells, repair of both regular and reduced abasic sites was increased with respect to normal extracts and was NAD+-independent, suggesting that in both short- and long-patch BER PARP-1 slows down, rather than stimulates, the repair reaction. Our data support the proposal that PARP-1 does not play a major role in catalysis of DNA damage processing via either base excision repair pathway.
Źródło:
Acta Biochimica Polonica; 2003, 50, 1; 169-179
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Bacterial DNA repair genes and their eukaryotic homologues: 2. Role of bacterial mutator gene homologues in human disease. Overview of nucleotide pool sanitization and mismatch repair systems
Autorzy:
Arczewska, Katarzyna
Kuśmierek, Jarosław
Powiązania:
https://bibliotekanauki.pl/articles/1040920.pdf
Data publikacji:
2007
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
MutT protein
human MutT homologue
DNA damage
mismatch repair
hereditary non-polyposis colorectal cancer
DNA repair
Opis:
Since the discovery of the first E. coli mutator gene, mutT, most of the mutations inducing elevated spontaneous mutation rates could be clearly attributed to defects in DNA repair. MutT turned out to be a pyrophosphohydrolase hydrolyzing 8-oxodGTP, thus preventing its incorporation into DNA and suppresing the occurrence of spontaneous AT→CG transversions. Most of the bacterial mutator genes appeared to be evolutionarily conserved, and scientists were continuously searching for contribution of DNA repair deficiency in human diseases, especially carcinogenesis. Yet a human MutT homologue - hMTH1 protein - was found to be overexpressed rather than inactivated in many human diseases, including cancer. The interest in DNA repair contribution to human diseases exploded with the observation that germline mutations in mismatch repair (MMR) genes predispose to hereditary non-polyposis colorectal cancer (HNPCC). Despite our continuously growing knowledge about DNA repair we still do not fully understand how the mutator phenotype contributes to specific forms of human diseases.
Źródło:
Acta Biochimica Polonica; 2007, 54, 3; 435-457
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Some aspects of the SOS response system - A critical survey.
Autorzy:
Janion, Celina
Powiązania:
https://bibliotekanauki.pl/articles/1044087.pdf
Data publikacji:
2001
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
SOS response
error-prone DNA polymerases
chronic SOS induction
DNA-repair
adaptive mutations
DNA mutations
Opis:
The SOS system and SOS mutagenesis are frequently studied, or exploited to obtain an increase in mutagenicity of bacteria. Here a short survey is made of the phenomenon of SOS response with special attention to latest and less discussed data, especially the induction of the SOS system in response to cell starvation or mutation of certain genes and the role of inducible DNA polymerases.
Źródło:
Acta Biochimica Polonica; 2001, 48, 3; 599-610
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Bacterial DNA repair genes and their eukaryotic homologues: 1. Mutations in genes involved in base excision repair (BER) and DNA-end processors and their implication in mutagenesis and human disease
Autorzy:
Krwawicz, Joanna
Arczewska, Katarzyna
Speina, Elzbieta
Maciejewska, Agnieszka
Grzesiuk, Elzbieta
Powiązania:
https://bibliotekanauki.pl/articles/1040919.pdf
Data publikacji:
2007
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
mutagenesis
AP endonuclease
SSBR
DNA damage
protein interaction
BER
DNA repair; glycosylase
SSB
Opis:
Base excision repair (BER) pathway executed by a complex network of proteins is the major system responsible for the removal of damaged DNA bases and repair of DNA single strand breaks (SSBs) generated by environmental agents, such as certain cancer therapies, or arising spontaneously during cellular metabolism. Both modified DNA bases and SSBs with ends other than 3'-OH and 5'-P are repaired either by replacement of a single or of more nucleotides in the processes called short-patch BER (SP-BER) or long-patch BER (LP-BER), respectively. In contrast to Escherichia coli cells, in human ones, the two BER sub-pathways are operated by different sets of proteins. In this review the selection between SP- and LP-BER and mutations in BER and end-processors genes and their contribution to bacterial mutagenesis and human diseases are considered.
Źródło:
Acta Biochimica Polonica; 2007, 54, 3; 413-434
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
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