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Determination of adenine nucleotides and their metabolites in human saliva.

100%
Kochańska B., Smoleński R. T., Knap N.
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2000
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vol. 47
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issue 3
877-879
EN
The profile and normal concentrations of nucleotide metabolites in human saliva and reproducibility of these determinations were analyzed. Samples of human saliva collected from healthy individuals at weekly intervals, were deproteinized and analysed for the content of adenine nucleotides and their metabolites by reversed-phase HPLC. Initial ATP, hypoxanthine and uric acid concentrations were 0.52 ± 0.15 μM, 1.91 ± 0.37 μM and 184 ± 22 μM respectively. A substantial individual variation persisted within 3 weeks of sampling excepted hypoxanthine which showed some unrelated variations. Determination of nucleotides and their catabolites in saliva due to its simplicity and reproducibility, may be of clinical value in diagnosis of local or systemic disorders.
2
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Dual effect of 2-methoxyestradiol on cell cycle events in human osteosarcoma 143B cells.

76%
Gołębiewska J., Rozwadowski P., Spodnik J. H., Knap N., Wakabayashi T., Woźniak M.
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2002
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vol. 49
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issue 1
59-65
EN
We have demonstrated for the first time that the steroid metabolite, 2-methoxyestradiol (2-ME) is a powerful growth inhibitor of human osteosarcoma 143 B cell line by pleiotropic mechanisms involving cell cycle arrest at two different points and apoptosis. The ability of 2-ME to inhibit cell cycle at the respective points has been found concentration dependent. 1 μM 2-ME inhibited cell cycle at G1 phase while 10 μM 2-ME caused G2/M cell cycle arrest. As a natural estrogen metabolite 2-ME is expected to perturb the stability of microtubules (MT) in vivo analogously to Taxol - the MT binding anticancer agent. Contrary to 2-ME, Taxol induced accumulation of osteosarcoma cells in G2/M phase of cell cycle only. The presented data strongly suggest two different mechanisms of cytotoxic action of 2-ME at the level of a single cell.
3
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Effect of pentoxifylline on proteinuria, markers of tubular injury and oxidative stress in non-diabetic patients with chronic kidney disease - placebo controlled, randomized, cross-over study

64%
Renke M., Tylicki L., Rutkowski P., Knap N., Ziętkiewicz M., Neuwelt A., Aleksandrowicz E., Łysiak-Szydłowska W., Woźniak M., Rutkowski B.
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2010
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vol. 57
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issue 1
119-123
EN
Background: Inhibition of the renin-angiotensin-aldosterone system (RAAS) with angiotensin converting enzyme inhibitors (ACEI) and/or angiotensin II subtype 1 receptor antagonists (ARB) is a common strategy used in the management of patients with chronic kidney disease (CKD). However, there is no universal therapy that can stop progression of CKD. Pentoxifylline (PTE) is a non-specific phosphodiesterase inhibitor with anti-inflammatory properties. It has been reported to have promising effects in CKD treatment. Methods: In a placebo-controlled, randomized, cross-over study we evaluated the influence of PTE (1200 mg/day) added to RAAS blockade on proteinuria, surrogate markers of tubular injury and oxidative stress-dependent products in 22 non-diabetic patients with proteinuria (0.4-4.3 g per 24h) with normal or declined kidney function [eGFR 37-178 mL/min]. In an eight-week run-in period, therapy using ACEI and/or ARB was adjusted to achieve a blood pressure below 130/80 mm Hg. Next, patients were randomly assigned to one of two treatment sequences: PTE/washout/placebo or placebo/washout/PTE. Clinical evaluation and laboratory tests were performed at the randomization point and after each period of the study. Results: The PTE therapy reduced proteinuria (by 26%) as compared to placebo. There were no differences in α1-microglobulin, urine excretion of N-acetyl-β-d-glucosaminidase (NAG), hsCRP, the urinary excretion of 15-F2t-isoprostane, blood pressure (BP), eGFR and serum creatinine between the PTE and placebo groups. Conclusion: Pentoxifylline may decrease proteinuria in non-diabetic patients with CKD.
4
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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.
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