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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.
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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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Background level of 8-oxo-2'-deoxyguanosine in lymphocyte DNA does not correlate with the concentration of antioxidant vitamins in blood plasma.

100%
Gackowski D., Ciecierski M., Jawień A., Oliński R.
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2001
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vol. 48
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issue 2
535-539
EN
Antioxidant vitamins, being effective free radical scavengers, can protect cellular DNA from oxidative damage. Therefore, in the present study we report on the relationship between basal level of 8-oxo-2'-deoxyguanosine in human lymphocyte DNA and the concentration of antioxidant vitamins (A, C and E). The average level of 8-oxo-2'-deoxyguanosine in lymphocytes of the studied group (15 males and 20 females) was 9.57 per 106 dG molecules. The endogenous level of ascorbic acid (vitamin C) in the plasma was, on average, 56.78 μM, while the mean concentrations of retinol (vitamin A) and α-tocopherol (vitamin E) were 1.24 μM and 25.74 μM, respectively. No correlations were found between individual 8-oxo-2'-deoxyguanosine levels in lymphocyte DNA and endogenous concentration of the vitamins.
3
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Lymphocyte labile iron pool, plasma iron, transferrin saturation and ferritin levels in colon cancer patients.

88%
Gackowski D., Kruszewski M., Banaszkiewicz Z., Jawien A., Olinski R.
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2002
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vol. 49
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issue 1
269-273
EN
Patients with colorectal carcinoma showed statistically significant lower values of transferrin saturation, total iron binding capacity and serum iron level as compared with control group, while the level of ferritin and the size of labile iron pool in carcinoma patients were higher, although this difference was not statistically significant. Our observations are in favour of the hypothesis which suggests that changes in iron metabolism restrict iron availability for tumour cells and as consequence, slow their growth.
4
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Oxidative damage to DNA and antioxidant status in aging and age-related diseases

64%
Olinski R., Siomek A., Rozalski R., Gackowski D., Foksinski M., Guz J., Dziaman T., Szpila A., Tudek B.
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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.
5
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Dynamics of estrogen-induced oxidative stress

52%
Kobiela J., Stefaniak T., Krajewski J., Kalinska-Blach B., Zurawa-Janicka D., Lachinski A., Gackowski D., Olinski R., Nowak J., Knap N., Lipinska B., Sledzinski Z., Wozniak M.
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2007
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vol. 54
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issue 2
289-295
EN
The objective of this study was to assess the dynamics of oxidative damage to cellular macromolecules such as proteins, lipids and DNA under conditions of oxidative stress triggering early stages of estrogen-dependent carcinogenesis. A rodent model of carcinogenesis was used. Syrian hamsters were sacrificed after 1, 3, 5 h and one month from the initial implantation of estradiol. Matching control groups were used. Kidneys as target organs for estradiol-mediated oxidative stress were excised and homogenized for biochemical assays. Subcellular fractions were isolated. Carbonyl groups (as a marker of protein oxidation) and lipid hydroxyperoxides were assessed. DNA was isolated and 8-oxodGuo was assessed. Electron paramagnetic resonance spectroscopy was used to confirm the results for lipid peroxidation. Exposition to estradiol in the rodent model leads to damage of macromolecules of the cell, including proteins and DNA, but not lipids. Proteins appear to be the primary target of the damage but are closely followed by DNA. It has previously been speculated that protein peroxides can increase DNA modifications. This time sequence was observed in our study. Nevertheless, the direct relation between protein and DNA damage still remains unsolved.
6
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Cu,Zn-superoxide dismutase deficiency in mice leads to organ-specific increase in oxidatively damaged DNA and NF-κB1 protein activity

52%
Siomek A., Brzoska K., Sochanowicz B., Gackowski D., Rozalski R., Foksinski M., Zarakowska E., Szpila A., Guz J., Bartlomiejczyk T., Kalinowski B., Kruszewski M., Olinski R.
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2010
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vol. 57
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issue 4
577-583
EN
Earlier experimental studies have demonstrated that: i) Cu,Zn-superoxide dismutase deficiency leads to oxidative stress and carcinogenesis; ii) dysregulation of NF-κB pathway can mediate a wide variety of diseases, including cancer. Therefore, we decided, for the first time, to examine the level of oxidative DNA damage and the DNA binding activity of NF-κB proteins in SOD1 knockout, heterozygous and wild-type mice. Two kinds of biomarkers of oxidatively damaged DNA: urinary excretion of 8-oxodG and 8-oxoGua, and the level of oxidatively damaged DNA were analysed using HPLC-GC-MS and HPLC-EC. The DNA binding activity of p50 and p65 proteins in a nuclear extracts was assessed using NF-κB p50/p65 EZ-TFA transcription factor assay. These parameters were determined in the brain, liver, kidney and urine of SOD1 knockout, heterozygous and wild-type mice. The level of 8-oxodG in DNA was higher in the liver and kidney of knockout mice than in wild type. No differences were found in urinary excretion of 8-oxoGua and 8-oxodG between wild type and the SOD1-deficient animals. The activity of the p50 protein was higher in the kidneys, but surprisingly not in the livers of SOD1-deficient mice, whereas p65 activity did not show any variability. Our results indicate that in Cu,Zn-SOD-deficient animals the level of oxidative DNA damage and NF-κB1 activity are elevated in certain organs only, which may provide some explanation for organ-specific ROS-induced carcinogenesis.
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