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1
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The protective ability of the Mediterranean plant extracts against the oxidative DNA damage. The role of the radical oxygen species and the polyphenol content

100%
Kapiszewska M., Soltys E., Visioli F., Cierniak A., Zajac G.
Journal of Physiology and Pharmacology. Supplement
|
2005
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tom 56
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nr 1
183-197
The polyphenol plant extracts content seems to be responsible for the scavenging activity of the reactive oxygen species (ROS), resulting in protection against DNA damage induced by the oxidative stress. This assumption was verified analyzing the effect of six Mediterranean plant extracts (Crepis vesicaria L, Origanum heracleoticum, Scandix australis L, Amaranthus sp., Scolymus hispanicus L, Thymus piperella L) on the oxidative DNA damage induced in lymphocytes by H2O2 in relation to the polyphenolic content and the lymphocyte scavenging ability of ROS. The comet assay was used to evaluate oxidative DNA damage and the polyphenol content was analyzed by the Folin-Ciocalteu method. The fluorescence resulting from oxidation of ROS-sensitive dye, dihydrorofluorescein (DHF), was utilized as indicator of the ROS level. Pretreatment with all plant extracts produced the dose-dependent increase in the DNA protection up to the 0.2 µg/ml polyphenol content and the decrease above that dose. Only the Thymus piperella, similarly to quercetin, showed a strong positive correlation between the DNA protection and the polyphenol content, but negative correlation with ROS formation. In conclusion, the DNA protective ability of plant extracts seems to be related to the low polyphenol concentration and only to certain extent depends on the polyphenol ROS scavenging activity.
2
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
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The estrogenic status and the COMT genotype of female blood donors influence the protective ability of the Mediterranean plant extracts against the hydrogen peroxide-induced DNA damage in lymphocytes

84%
Kapiszewska M., Zajac G., Kalemba M., Soltys E.
Journal of Physiology and Pharmacology. Supplement
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2005
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tom 56
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nr 1
199-217
The extent of oxidative DNA damage in lymphocytes can be used as a biomarker of the level of oxidative stress in the body. The comet assay has been widely used to measure such damage. The aim of our study was to evaluate: i) the extent of the oxidative DNA damage in lymphocytes isolated from blood of female donors taken in early and late follicular phases [low (LE) and high (HE) concentration of 17bestradiol, respectively], ii) the susceptibility of these lymphocytes to hydrogen peroxide exposure, and iii) the protective ability of five plant extracts against the hydrogen peroxide-induced DNA damage. The effect of the catechol-Omethytransferase genotype (wild COMT H/H and mutated homozygote COMT L/L) of female donors was also analyzed. The amount of endogenous DNA damage was higher in HE lymphocytes as compared with LE ones, independently of the genotype. When lymphocytes were stratified by COMT genotype, the level of DNA damage was higher in L/L donors. The protective effect of pretreatment with plant extracts (1 and 10 µg/ml for 1 h) against the H2O2 (25 µM, 5 min. at 4°C)-induced oxidative DNA damage was observed only in H/H HE lymphocytes. In contrary, the plant extract pre-incubation enhanced the DNA damage in L/L HE lymphocytes. The plant extracts alone did not induce the DNA damage. The results showed that concentration of the circulating 17b-estradiol influenced the extent of endogenous oxidative DNA damage while the beneficial or hazardous effects of the plant extracts might depend on the COMT genotype and the estrogen level.
3

Cellular level of 8-oxo-2'-deoxyguanosine in DNA does not correlate with urinary excretion of the modified base nucleoside

84%
Foksinski M., Gackowski D., Rozalski R., Olinski R.
Acta Biochimica Polonica
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2003
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tom 50
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nr 2
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.
4

A comparison of the in vitro genotoxicity of anticancer drugs idarubicin and mitoxantrone

84%
Blasiak J., Gloc E., Warszawski M.
Acta Biochimica Polonica
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2002
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tom 49
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nr 1
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 uM 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 uM 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.
5
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Standardized Tribulus terrestris extract protects against rotenone-induced oxidative damage and nigral dopamine neuronal loss in mice

67%
Alzahrani S., Ezzat W., Elshaer R. E., Abd El-Lateef A. S., Mohammad H. M. F., Elkazaz A. Y., Toraih E., Zaitone S. A.
Journal of Physiology and Pharmacology
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2018
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tom 69
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nr 6
6

Increased salivary level of 8-hydroxydeoxyguanosine is a marker of premature oxidative mitochondrial DNA damage in gingival tissue of patients with periodontitis

67%
Canakci C. F., Canakci V., Tatar A., Eltas A., Sezer U., Cicek Y., Oztas S.
Archivum Immunologiae et Therapiae Experimentalis
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2009
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tom 57
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nr 3
205-211
7

Occupational noise exposure may induce oxidative DNA damage

67%
Nawaz S. K., Hasnain S.
Polish Journal of Environmental Studies
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2013
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tom 22
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nr 5
Occupational noise enhances the risk of several cardiovascular and non-cardiovascular diseases. The reason behind the drastic effects of noise exposure is the excessive generation of reactive oxygen species molecules. The present study investigates oxidative stress due to occupational noise exposure in 192 male smoking workers exposed to normal noise (sound level ≤80 dBA), low noise (sound level 81-94 dBA), and loud noise (sound level ≥95 dBA). University-aged volunteers were selected for the normal sound exposed group. Drivers and conductors were selected for the low-noise exposed group, and workers of power loom factories were chosen for the high-noise exposed group. Oxidative stress was estimated using 8 OHdG as a biomarker for oxidative DNA damage. Serum aldosterone and serum cortisol level was estimated using the enzyme immunoassay method. Results indicated that 8 OHdG level was significantly different in different exposure groups. It was highest in the low-noise exposed group (0.370±0.017 ng/ml) and lowest in the normal-sound exposed group (0.22±0.01 ng/ml). Level of 8 OHdG in the high-noise exposed group was 0.29±0.00. There was no significant variation of aldosterone levels among different groups. Cortisol levels of both noise groups was higher than that of the normal sound group. It can be concluded that noise exposure induces stress in the Pakistani population. This stress leads to oxidative DNA damage.
8

Oxidative damage to DNA and antioxidant status in aging and age-related diseases

67%
Olinski R., Siomek A., Rozalski R., Gackowski D., Foksinski M., Guz J., Dziaman T., Szpila A., Tudek B.
Acta Biochimica Polonica
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2007
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tom 54
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nr 1
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.
9
Content available remote

Modulation of oxidative DNA damage repair by the diet, inflammation and neoplastic transformation

59%
Tudek B., Swoboda M., Kowalczyk P., Olinski R.
Journal of Physiology and Pharmacology. Supplement
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2006
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tom 57
|
nr 7
33-49
Oxidative DNA damage and DNA repair may mediate several cellular processes, like replication and transcription, mutagenesis and apoptosis and thus may be important for the organism development as well as its pathogenesis, including cancer. Activity of DNA repair enzymes can depend on many factors, such as gene polymorphism, mRNA and protein level, as well as enzymes activation and inhibition. Modulation of base excision repair pathway eliminating from DNA oxidatively formed lesions may be caused by the diet, inflammation and neoplastic transformation. Reactive oxygen species and some diet components induce transcription of several Base Excision Repair enzymes, e.g. major human AP-endonuclease, (APE1) and 8-oxoG-DNA glycosylase (OGG1). The carcinogenic process in human lungs decreases repair activity for 8-oxoG in transcription independent manner, but increases repair activity of eA and eC, as measured in tumors and unchanged lung tissues of lung cancer patients. Thus, modulation of repair enzymes activities may be a cell response on their way to differentiation or neoplastic transformation.
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