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Wyświetlanie 1-13 z 13
Tytuł:
The effect of quercetin on oxidative DNA damage and myelosuppression induced by etoposide in bone marrow cells of rats
Autorzy:
Papież, Monika
Powiązania:
https://bibliotekanauki.pl/articles/1039316.pdf
Data publikacji:
2014
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
quercetin
etoposide
myelosuppression
oxidative DNA damage
comet assay
Opis:
There is increasing evidence for the existence of an association between the presence of etoposide phenoxyl radicals and the development of treatment-related acute myeloid leukemia (t-AML), which occurs in a few percent of patients treated with this chemotherapeutic agent. The most common side effect caused by etoposide is myelosuppression, which limits the use of this effective drug. The goal of the study was to investigate the influence of antioxidant querectin on myelosuppression and oxidative DNA damage caused by etoposide. The influence of quercetin and/or etoposide on oxidative DNA damage was investigated in LT-12 cell line and bone marrow cells of rats via comet assay. The effect of quercetin on myelosuppression induced by etoposide was invetsigated by cytological analysis of bone marrow smears stained with May-Grünwald-Giemsa stain. Etoposide caused a significant increase in oxidative DNA damage in bone marrow cells and LT-12 cell line in comparison to the appropriate controls. Quercetin significantly reduced the oxidative DNA damage caused by etoposide both in vitro and in vivo. Quercetin also significantly protected against a decrease in the percentage of myeloid precursors and erythroid nucleated cells caused by etoposide administration in comparison to the group treated with etoposide alone. The results of the study indicate that quercetin could be considered a protectively acting compound in bone marrow cells during etoposide therapy.
Źródło:
Acta Biochimica Polonica; 2014, 61, 1; 7-11
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:
Cellular level of 8-oxo-2-deoxyguanosine in DNA does not correlate with urinary excretion of the modified base/nucleoside.
Autorzy:
Foksinski, Marek
Gackowski, Daniel
Rozalski, Rafał
Olinski, Ryszard
Powiązania:
https://bibliotekanauki.pl/articles/1043637.pdf
Data publikacji:
2003
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
8-oxoguanine
oxidative DNA damage
8-oxo-2'-deoxyguanosine
Opis:
We assessed a relationship between the level of 8-oxodG in leukocyte DNA measured with the high performance liquid chromatography with electrochemical detection (HPLC/EC) technique and urinary excretion of the modified nucleoside/base analysed with a recently developed methodology involving HPLC prepurification followed by gas chromatography with isotope dilution mass spectrometric detection. No correlation was found between these markers of oxidative DNA damage commonly used in epidemiological studies. Several possible explanations of this finding are discussed.
Źródło:
Acta Biochimica Polonica; 2003, 50, 2; 549-553
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Oxidative damage to DNA and antioxidant status in aging and age-related diseases
Autorzy:
Olinski, Ryszard
Siomek, Agnieszka
Rozalski, Rafal
Gackowski, Daniel
Foksinski, Marek
Guz, Jolanta
Dziaman, Tomasz
Szpila, Anna
Tudek, Barbara
Powiązania:
https://bibliotekanauki.pl/articles/1041102.pdf
Data publikacji:
2007
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
ROS
aging
oxidative DNA damage
age-related diseases
BER
GO system
Opis:
Aging is a complex process involving morphologic and biochemical changes in single cells and in the whole organism. One of the most popular explanations of how aging occurs at the molecular level is the oxidative stress hypothesis. Oxidative stress leads in many cases to an age-dependent increase in the cellular level of oxidatively modified macromolecules including DNA, and it is this increase which has been linked to various pathological conditions, such as aging, carcinogenesis, neurodegenerative and cardiovascular diseases. It is, however, possible that a number of short-comings associated with gaps in our knowledge may be responsible for the failure to produce definite results when applied to understanding the role of DNA damage in aging and age-related diseases.
Źródło:
Acta Biochimica Polonica; 2007, 54, 1; 11-26
0001-527X
Pojawia się w:
Acta Biochimica Polonica
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:
The cryoprotective potential of propolis supplemented in frozen-thawed bull semen; biochemical and physiological findings
Autorzy:
Yeni, D.
Gülhan, M.F.
İnanç, M.E.
Avdatek, F.
Güngör, Ş.
Türkmen, R.
Tuncer, P.B.
Taşdemir, U.
Powiązania:
https://bibliotekanauki.pl/articles/16539069.pdf
Data publikacji:
2022
Wydawca:
Polska Akademia Nauk. Czasopisma i Monografie PAN
Tematy:
cryopreservation
DNA damage
oxidative stress
propolis
Opis:
In this study, the cryoprotective effect of different doses of propolis (P) on bull semen, which has solid pharmacological properties thanks to its rich phenolic components, was investigated biochemically and physiologically. Semen samples were collected from Simmental breed bulls via the artificial vagina and pooled. After dividing into five groups, control (C: no additive) and four different P (200, 100, 50, and 25 μg/mL) groups, the final concentration was diluted to 16×106 per straw. Semen samples were equilibrated at 4°C for approximately 4 hours, then placed in French straws and frozen. After thawing, sperm motility and kinetic parameters, DNA integrity by single-cell gel electrophoresis, sperm abnormalities by liquid fixation, and lipid peroxidation levels by the colorimetric method was analyzed by Computer-Assisted Semen Analyzer. P added to the diluent showed no effect on motility and kinetic parameters at P25 and P50 (p>0.05), while P100 and P200 had a negative effect (p<0.001). The addition of P (25 and 50) showed a treatment effect on tail abnormality compared to C (p<0.05). Especially P50 had a positive effect on tail length, tail DNA, and tail movement, while P100 and P200 caused DNA damage (p<0.001). MDA levels increased in all P dose groups compared to C (p<0.001). This study has clearly demonstrated that P25 and P50 supplements could be used therapeutically to treat sperm tail abnormalities and prevent DNA damage in post-thawed bull sperm.
Źródło:
Polish Journal of Veterinary Sciences; 2022, 25, 1; 5-12
1505-1773
Pojawia się w:
Polish Journal of Veterinary Sciences
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Identification of health risks from harmful chemical agents - review concerning bisphenol A in workplace
Autorzy:
Kapustka, Katarzyna
Ziegmann, Gerhard
Klimecka-Tatar, Dorota
Ostrega, Mateusz
Powiązania:
https://bibliotekanauki.pl/articles/1839518.pdf
Data publikacji:
2020
Wydawca:
Stowarzyszenie Menedżerów Jakości i Produkcji
Tematy:
bisphenol A
health risk
harmful chemical agents
human exposure
DNA oxidative damage
bisfenol A
ryzyko dla zdrowia
szkodliwe środki chemiczne
narażenie ludzi
uszkodzenie oksydacyjne DNA
Opis:
Bisphenol A (BPA) is an industrial chemical used as an additive in conventional point-of-sale thermal paper receipts, in the production of many polycarbonate plastics, and epoxy resins lignin for food. BPA is xenoestrogen, a foreign compound that is not naturally produced in living organisms, but which acts similarly to natural 17-ß estradiol (natural estrogen). Due to its weak estrogenic activities, BPA exposure may influence multiple endocrine-related pathway, and is associated with prostate and breast cancer, neurobehavioral deficits, heart disease, and obesity. Furthermore, BPA may act as a DNA methylation agent and cause altered gene expression in the brain. Human exposure to bisphenol A is a matter of controversy. This review shows a potential risks in workplace resulting from contact with bisphenol A. The work presents the contribution of BPA exposure levels via dermal contact and the relationship between BPA exposure level and oxidative DNA damage.
Źródło:
Production Engineering Archives; 2020, 26, 2; 45-49
2353-5156
2353-7779
Pojawia się w:
Production Engineering Archives
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:
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:
Association between body iron stores and level of oxidatively modified DNA bases
Autorzy:
Dziaman, T.
Jurgowiak, M.
Olinski, R.
Powiązania:
https://bibliotekanauki.pl/articles/80695.pdf
Data publikacji:
2011
Wydawca:
Polska Akademia Nauk. Czytelnia Czasopism PAN
Tematy:
atherosclerosis
cancer
cardiovascular disease
cellular DNA
free radical damage
heterozygosity
iron deficiency anaemia
labile iron pool
oxidative damage
oxidative stress
reactive oxygen species
vascular disease
Źródło:
BioTechnologia. Journal of Biotechnology Computational Biology and Bionanotechnology; 2011, 92, 2
0860-7796
Pojawia się w:
BioTechnologia. Journal of Biotechnology Computational Biology and Bionanotechnology
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Molecular mechanisms of lead toxicity
Autorzy:
Szymanski, M.
Powiązania:
https://bibliotekanauki.pl/articles/80273.pdf
Data publikacji:
2014
Wydawca:
Polska Akademia Nauk. Czytelnia Czasopism PAN
Tematy:
lead toxicity
molecular mechanism
heavy metal
oxidative stress
DNA damage
calcium binding protein
zinc finger protein family
DNA methylation
Źródło:
BioTechnologia. Journal of Biotechnology Computational Biology and Bionanotechnology; 2014, 95, 2
0860-7796
Pojawia się w:
BioTechnologia. Journal of Biotechnology Computational Biology and Bionanotechnology
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:
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
    Wyświetlanie 1-13 z 13

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