Titlebook: Cellular Effects of Heavy Metals; Gaspar Banfalvi Book 2011 Springer Science+Business Media B.V. 2011 accumulation.apoptosis.carcinogenesi

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pects of environmental hazard, ecosystems and human health. Among the cellular responses of heavy metals irregularities in cellular mechanisms such as gene expression, protein folding, stress signaling pathways978-94-007-9225-8978-94-007-0428-2

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Book 2011oxic, mutagenic and carcinogenic effects. The toxicity of several metals touch upon the aspects of environmental hazard, ecosystems and human health. Among the cellular responses of heavy metals irregularities in cellular mechanisms such as gene expression, protein folding, stress signaling pathways

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Toxic Metal/Metalloid Tolerance in Fungi—A Biotechnology-Oriented Approachracellular metal chelators, (v) overproduction of elements of the antioxidative defense system, (vi) genetic modification of the regulatory network of metal/metalloid stress defense, and (vii) interfering with the metal/metalloid-dependent initialization of apoptotic cell death. Owing to the wide-sp

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Interference of Chromium with Cellular Functions transport of Cr(VI) and Cr(III) through non-selective and selective ion channels and yeast chromium mutants that are able to take up very low concentrations of chromium. This uptake-reduction model helps to explain the generation of reactive oxygen species (ROS), which are primarily responsible for

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Chromatin Toxicity of Ni(II) Ions in K562 Erythroleukemia Cellsion 1?μM NiCl. generated larger apoptotic chromatin circles. At 5?μM NiCl. the slight expansion of nuclei and the continuous chromatin ribbon became visible. At 10?μM Ni(II) most of the nuclear material condensed prematurely, the rest remained in highly decondensed fibrillary stage. Necrotic changes

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Role of Oxidative Damage in Metal-Induced Carcinogenesisicity of DNA base products, strand breaks, apurinic sites, cross-links, and adducts typical for the attacking reactive species (oxygen-, carbon-, or sulfur-centered radicals), originating from oxidized amino acids and proteins, and 4-hydroxynonenal, a lipid oxidation product. Oxidative damage to nuc