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

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書目名稱Cellular Effects of Heavy Metals
編輯Gaspar Banfalvi
視頻videohttp://file.papertrans.cn/224/223022/223022.mp4
概述Describes the biological importance of heavy metals.Shows how heavy metals enter cells.What happens inside the cells upon heavy metal uptake.What chemical reactions are induced by heavy metals.What me
圖書封面Titlebook: Cellular Effects of Heavy Metals;  Gaspar Banfalvi Book 2011 Springer Science+Business Media B.V. 2011 accumulation.apoptosis.carcinogenesi
描述.The term “heavy metals” is used as a group name of toxic metals and metalloids (semimetals) causing contaminations and ecotoxicity. In strict chemical sense the density of heavy metals is higher than 5 g/cm3. From biological point of view as microelements they can be divided into two major groups. a. For their physiological function organisms and cells require essential microelements such as iron, chromium (III), cobalt, copper, manganese, molidenium, zinc. b. The other group of heavy metals is toxic to the health or environment. Of highest concern are the emissions of As, Cd, Co, Cu, Hg, Mn, Ni, Pb, Sn, Tl. The toxicity of heavy metals is well known at organizational level, while less attention has been paid to their cellular effects. This book describes the toxicity of heavy metals on microorganisms, yeast, plant and animal cells. Other chapters of the book deal with their genotoxic, 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
出版日期Book 2011
關(guān)鍵詞accumulation; apoptosis; carcinogenesis; genotoxicity; removal; ecotoxicology
版次1
doihttps://doi.org/10.1007/978-94-007-0428-2
isbn_softcover978-94-007-9225-8
isbn_ebook978-94-007-0428-2
copyrightSpringer Science+Business Media B.V. 2011
The information of publication is updating

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as a Model Organism for Elucidating Arsenic Tolerance Mechanisms of key yeast proteins involved in arsenite accumulation and efflux, arsenate reduction, and the use of complementation assays where a yeast protein is replaced by a homologous protein from another organism, has accelerated the identification of arsenic tolerance genes in fungi, plants, animals, and
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Heavy Metal Toxicity in an Insect Cell Line (Methyl-HgCl, HgCl2, CdCl2 and CuSO4)proliferation was drastically inhibited by CdCl. and MeHgCl while HgCl. showed only a moderate effect. Acute toxicity tests showed that membrane integrity was severely affected in cells treated with low doses of HgCl. and MeHgCl. Uptake of both mercury species occurred via simple diffusion while cad
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Cellular Changes in Mammalian Cells Induced by Cadmiumreplication, DNA repair) and morphological (chromatin) changes in CHO and murine preB cells. Low Cd concentration (0.5–1?μM) interferes with both replicative and repair DNA synthesis. The replicative DNA synthesis is gradually inhibited, but this inhibition is less than the increment of repair DNA s
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Heavy Metal-Induced Carcinogenicity: Depleted Uranium and Heavy-Metal Tungsten Alloy whose toxicological properties may not as yet be well-understood. This chapter reviews what is currently known about two recent additions to many nations’ arsenals: depleted uranium and heavy-metal tungsten alloy. The toxicological and genotoxic properties of these materials, derived from both . an
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