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1

Quantitative determination of oxidative base damage in DNA

100%
Zastawny T. H.
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vol. 49
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issue 5
609-630
EN
Oxidative DNA damage produced by free radicals has been implicated to play a role in mutagenesis, carcinogenesis and aging.There is, therefore, increasing interest in teh development of accurate assays for measuring DNA base damage.Such assays should help to define the biological consequences of oxidative DNA modifications and to identify enzymatic repair pathways.The present article describes the potential usefulness of different technique for chemical characterizatoin and quantitation of ixidative modifications in DNA.
2

Nucleotide excision repair, NER - a relationship with cancer risk

80%
Butkiewicz D., Rusin M., Pawlas M., Czarny M., Chorazy M.
Postępy Higieny i Medycyny Doświadczalnej
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2002
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vol. 56
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issue 4
485-498
EN
DNA damage repair, responsible for maintaining the genome integrity, plays a central role in cancer biology. Individual DNA repair capacity is genetically determined. Inherited defect in nucleotide excision repair (NER) genes leads to three distinct and extremely rare disorders: xeroderma pigmentosum, associated with high risk of skin cancer, Cockayne syndrome, and trichothiodystrophy. The recently identified common polymorphism in several NER genes may also influence a risk of cancer in general population. The review presents current knowledge about a role of genetic variation of NER genes in cancer predisposition.
3

DNA damage by active species and its role in carcinigenesis

80%
Olinski R.
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vol. 47
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issue 6
463-473
4

Manifestations of ageing at the cytogenetic level

80%
Wojda A., Witt M.
Journal of Applied Genetics
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2003
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vol. 44
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issue 3
383-399
EN
The effects of ageing in humans appear to be a combination of influence of genetically programmed phenomena and exogenous environmental factors, and take place at the cellular level (senescence), rather than at the level of the organism. There are many processes, which occur in somatic cells as a consequence of DNA replication (accumulation of DNA errors or mutations that outstrip repair processes, telomere shortening, deregulation of apoptosis, etc.) and which drive replicative senescence in human cells. DNA errors are considered to be critical primary lesions in the formation of chromosomal aberrations. It can be concluded that the chromosome aberrations are biomarkers of ageing in human cells. Studies of human metaphases, interphase nuclei and micronuclei showed the increase in loss of chromosomes and the increase in frequency of stable chromosome aberrations as a function of age.
5
Content available remote

Amyloid beta protein affects poly(ADP-ribose) polymerase activity in PC-12 cells in culture

80%
Strosznajder R. P., Banasik M.
Acta Neurobiologiae Experimentalis
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2000
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vol. 60
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issue 2
215
6

Mystery of DNA repair: the role of the MRN complex and ATM kinase in DNA damage repair

70%
Czornak K., Chughtai S., Chrzanowska K. H.
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EN
Genomes are subject to a number of exogenous or endogenous DNA-damaging agents that cause DNA double-strand breaks (DSBs). These critical DNA lesions can result in cell death or a wide variety of genetic alterations, including deletions, translocations, loss of heterozygosity, chromosome loss, or chromosome fusions, which enhance genome instability and can trigger carcinogenesis. The cells have developed an efficient mechanism to cope with DNA damages by evolving the DNA repair machinery. There are 2 major DSB repair mechanisms: nonhomologous end joining (NHEJ) and homologous recombination (HR). One element of the repair machinery is the MRN complex, consisting of MRE11, RAD50 and NBN (previously described as NBS1), which is involved in DNA replication, DNA repair, and signaling to the cell cycle checkpoints. A number of kinases, like ATM (ataxia-telangiectasia mutated), ATR (ataxia-telangiectasia and Rad-3-related), and DNA PKcs (DNA protein kinase catalytic subunit), phosphorylate various protein targets in order to repair the damage. If the damage cannot be repaired, they direct the cell to apoptosis. The MRN complex as well as repair kinases are also involved in telomere maintenance and genome stability. The dysfunction of particular elements involved in the repair mechanisms leads to genome instability disorders, like ataxia telangiectasia (A-T), A-T-like disorder (ATLD) and Nijmegen breakage syndrome (NBS). The mutated genes responsible for these disorders code for proteins that play key roles in the process of DNA repair. Here we present a detailed review of current knowledge on the MRN complex, kinases engaged in DNA repair, and genome instability disorders.
7

Documenting ancient DNA quality via alpha satellite amplification and assessment of clone sequence diversity

70%
Pusch C. M., Kayademir T., Prangenberg K., Conard N. J., Czarnetzki A., Blin N.
Journal of Applied Genetics
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2002
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vol. 43
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issue 3
351-363
EN
C/GT/A nucleotide alterations have been shown to hamper the straightforward interpretation of mitochondrial DNA sequence data derived from ancient tissues. Attempting to characterise this finding with respect to nuclear DNA, we contrasted two established protocols: (i) an enzymatic repair of damaged DNA, thereby translating and closing nicks in the DNA, and (ii) the application of N-phenacylthiazolium bromide, which cleaves glucose-derived protein crosslinks, presumably derived from Maillard reactions. We used medieval human bones that were refractory to standard PCR procedures. Due to negligible presence of short tandem repeat loci and also mitochondrial sequences, the extracted ancient DNA needed a higher copy PCR system to yield amplification products. The chosen PCR target was specific alphoid repetitive DNA with an experimentally determined minimum of 1000 copies per haploid genome. Alphoid repeat segments were generated from both contemporary DNA and DNA extracts of two human skeletons dating from 450-600 AD (omitting uracil N-glycosylase pre-treatment of the extracted samples), and were subsequently cloned and sequenced. The sequences were evaluated for the number and type of nucleotide alterations noted after the different pre-treatments, and were compared to our alphoid consensus sequence generated from modern DNA. Both methods failed to reflect the expected 32% variability among single alphoid repeats (accounting for locus-specific differences and polymerase errors) as well as to display the actual 2.88 ratio of transitions to transversions. Our data obtained from high-copy-number nuclear DNA mirror the phenomenon of sequence deviations observed in mitochondrial DNA extracted from old specimens.
8

DNA damage and repair after exposure to sevoflurane in vivo, evaluated in Swiss albino mice by the alkaline comet assay and micronucleus test

61%
Brozovic G., Orsolic N., Rozgaj R., Kasuba V., Knezevic F., Knezevic A. H., Benkovic V., Lisicic D., Borojevic N., Dikic D.
Journal of Applied Genetics
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2010
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vol. 51
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issue 1
79-86
EN
The relationship between DNA damage and repair of peripheral blood leukocytes, liver, kidney and brain cells was investigated in Swiss albino mice (Mus musculus L.) after exposure to sevoflurane (2.4 vol% for 2 h daily, for 3 days). Genetic damage of mouse cells was investigated by the comet assay and micronucleus test. To perform the comet assay, mice were divided into a control group and 4 groups of exposed mice sacrificed on day 3 of the experiment, at 0, 2, 6 or 24 h after the last exposure to sevoflurane. Mean tail length (TL), tail moment (TM), and tail intensity (TI) values were significantly higher in exposed mice (all examined organs) than in the control group. Significant DNA damage immediately after exposure to sevoflurane was observed in leukocytes. Damage induction in the liver, kidney, and brain occurred 6 h later than in leukocytes, as expected according to the toxicokinetics of the drug, where blood is the first compartment to absorb sevoflurane. However, none of the tested tissues revealed signs of repair until 24 h after the exposure. To distinguish the unrepaired genome damage in vivo, the micronucleus test was applied. Number of micronuclei in reticulocytes showed a statistically significant increase, as compared with the control group at all observed times after the treatment.
9

Cytogenetic perspective of ageing and longevity in men and women

51%
Zietkiewicz E., Wojda A., Witt M.
Journal of Applied Genetics
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2009
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vol. 50
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issue 3
261-273
EN
Analysis of relationships between the ageing cell phenotype and the age of cell donors is one of the ways towards understanding the link between cellular and organismal ageing. Cytogenetically, ageing is associated with a number of gross cellular changes, including altered size and morphology, genomic instability, and changes in expression and proliferation. Genomic instability can be easily assessed by analyzing the level of cytogenetic aberrations. In this review, we focus on the differences in the level and profile of cytogenetic aberrations observed in donors of different age and gender. Centenarians are a small fraction of the population at the extreme of human longevity. Their inclusion in such studies may shed light on one of the basic questions: whether genome stability is better maintained in successfully aged individuals compared to the rest of the population. At the same time, comparing the profile of age-related amount of chromosomal aberrations in men and women may help explaining the commonly observed gender differences in longevity.
10
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Aneuploidy, chromosomal missegregation, and cell cycle reentry in Alzheimer's disease

51%
Zekanowski C., Wojda U.
Acta Neurobiologiae Experimentalis
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2009
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vol. 69
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issue 2
232-253
EN
Alzheimer's disease (AD) is a neurodegenerative disorder with a complex etiology and pathogenesis. Chromosome missegregation was proposed two decades ago to be responsible for neurodegeneration in AD patients. It was speculated that the aneuploidy is a result of aberrant cell cycle of neuronal progenitors during adult neurogenesis and/or of mature neurons. There is mounting evidence of increased rate of general aneuploidy and cell cycle reentry in the AD patients' brains, with area-specific pattern. In this review, we discuss the involvement of chromosome instability, genome damage and cell cycle impairment in AD pathology.
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