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1
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Cellular level of 8-oxo-2'-deoxyguanosine in DNA does not correlate with urinary excretion of the modified base/nucleoside.

100%
Foksinski M., Gackowski D., Rozalski R., Olinski R.
Acta Biochimica Polonica
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2003
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vol. 50
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issue 2
549-553
EN
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.
2
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The effect of quercetin on oxidative DNA damage and myelosuppression induced by etoposide in bone marrow cells of rats

88%
Papież M.
Acta Biochimica Polonica
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2014
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vol. 61
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issue 1
7-11
EN
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.
3
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Changes in Urinary 8-Hydroxydeoxyguanosine Levels During Heptathlon Race in Professional Female Athletes

88%
Samia B. A. A., Youssef G. A.
Journal of Human Kinetics
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2014
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vol. 41
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issue 1
107-111
EN
Acute strenuous exercise can induce a state of oxidative stress affecting the involved muscles. Heptathlon is a multi-event exercise of two days duration and can be considered an acute, intensive endurance exercise. The purpose of this study is to compare the oxidative stress response to heptathlon events day by day and to determine the impact of this type of exercise on oxidative stress biomarkers. The study subjects included eight heptathlon athletes who participated in the National First Class Republic competition in Egypt (October 19-21, 2011). Blood samples were collected at rest after exercise for two successive days and analyzed for malondialdehyde (MDA). Morning urine samples were collected one hour after exercise for each day and were analyzed for 8-hydroxydeoxyguanosine (8-OHdG). Results revealed a significant increase (p<0.05) in both plasma MDA and urine 8-OHdG levels after exercise regardless of the day. We concluded that exercise generates higher MDA levels compared to DNA strand breaks and oxidative DNA damage in athletes with antioxidant supplementation.
4
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A comparison of the in vitro genotoxicity of anticancer drugs idarubicin and mitoxantrone.

75%
Błasiak J., Gloc E., Warszawski M.
Acta Biochimica Polonica
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2002
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vol. 49
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issue 1
145-155
EN
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.
5
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Oxidative damage to DNA and antioxidant status in aging and age-related diseases

75%
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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vol. 54
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issue 1
11-26
EN
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.
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