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nr 6
691-705
EN
This review concerns a brief introduction into the basics of tumor blood vessels development as well as the regulatory mechanisms of this process. The role of copper ions in tumor angiogenesis is discussed. The new antiangiogenic therapies based on a reduction of copper levels in tumor microenvironment are reviewed.
EN
Curcumin is a phytochemical with antiinflammatory, antioxidant and anticarcinogenic activities. Apparently, curcumin is not genotoxic in vivo, but in vitro copper and curcumin interactions induce genetic damage. The aim of this study was to test if in vivo copper excess induces DNA damage measured by comet and micronucleus assays in the presence of curcumin. We tested 0.2% curcumin in Balb-C mice at normal (13 ppm) and high (65, 130 and 390 ppm) copper ion concentrations. The comet and micronucleus assays were performed 48 hr after chemical application. Comet tail length in animals treated with 0.2% curcumin was not significantly different from the control. Animals exposed to copper cations (up to 390 ppm) exhibited higher oxidative DNA damage. Curcumin reduced the DNA damage induced by 390 ppm copper. We observed statistically significant increase in damage in individuals exposed to 390 ppm copper versus the control or curcumin groups, which was lowered by the presence of curcumin. Qualitative data on comets evidenced that cells from individuals exposed to 390 ppm copper had longer tails (categories 3 and 4) than in 390 ppm copper + curcumin. A statistically significant increase in frequency of micronucleated erythrocytes (MNE/10000TE) was observed only in 390 ppm copper versus the control and curcumin alone. Also cytotoxicity measured as the frequency of polychromatic erythrocytes (PE/1000TE) was attributable to 390 ppm copper. The lowest cytotoxic effect observed was attributed to curcumin. In vivo exposure to 0.2% curcumin for 48 hr did not cause genomic damage, while 390 ppm copper was genotoxic, but DNA damage induced by 390 ppm copper was diminished by curcumin. Curcumin seems to exert a genoprotective effect against DNA damage induced by high concentrations of copper cations. The comet and micronucleus assays prove to be suitable tools to detect DNA damage by copper in the presence of curcumin.
EN
The Domiaza is a fragment of the Oder river estuary situated north of Szczecin. This area is exposed to complex hydrological processes and strong anthropogenic pressure. Key physical and chemical parameters of the Domiaza sediments (fraction < 2mm), e.g., dry residue (Ds), ignition loss (Iz), CaCO3 and organic carbon content, show high coefficients of variation (over 60%). Similar variation is typical of the heavy metal concentrations (Cu, Zn, Pb, Co, Cd and Hg) and the organic carbon content in the fraction smaller than 0.20 mm. The spatial distribution of the examined parameters in the Domiaza sediments results from the dynamics of this environment, especially the heavy watercraft traffic and the continuous dredging of the Szczecin-Swinoujscie water lane. Concentrations of Cd, Cu, Zn, Pb and Co found in the Domiaza sediments are higher than those found in the geochemical background of Poland, while concentrations of mercury are comparable. Moreover, the concentrations of Cu, Zn, Pb and Cd found in the Domiaza sediments are higher than the average concentrations of these metals in adjacent areas (Oder River, Dabie Lake, Szczecin Lagoon), but the concentrations of Hg and Co are comparable or lower depending on the area of reference. A survey of heavy metals concentrations conducted in 1999 detected higher than average concentrations of Cu, Zn, Pb, and particularly Co (twice) and Hg (over thirty times), and lower concentrations of Cd in comparison with the average levels of 1996. The reason for these differences was the selective inflow of heavy metals to the Domiaza area after the disastrous flood of 1997.
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nr 2
131-145
EN
This mini review gives a brief overview over the oxidation mechanism of methionine (Met), relevant for processes which may lead to the oxidation of amyloid beta-peptide (betaAP), involved in the pathogenesis of Alzheimer?s disease. The Cu II-catalysed oxidation of C-terminal Met 35 in AP depends on the secondary structure of the peptide. That seems to be the key to the known propensities of this peptide to form reactive oxygen species and free radicals. The pro-oxidant character of betaAP is not associated with its -beta sheet insoluble form. On the contrary, the alpha-helically organised structure is responsible for betaAP redox-related cytotoxicity.
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