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pubmed-article:10933881pubmed:abstractTextThe lipophilic copper(I)-specific chelator neocuproine has been frequently used as an inhibitor of copper-mediated damage in biological systems. In this communication we report that the copper-mediated toxicity of 2,4,5-trichlorophenol is markedly potentiated by neocuproine at levels which are near-stoichiometric with respect to the copper concentration but is inhibited at higher concentrations. However, no potentiation was observed when neocuproine was substituted by bathocuproinedisulfonic acid, a negative charged ligand with essentially the same copper-binding characteristics as neocuproine. We found that the potentiation by neocuproine was due to the formation of a lipophilic copper complex, while the inhibition by bathocuproinedisulfonic acid was due to the formation of a hydrophilic one. Caution in the use of neocuproine to study copper-mediated toxicity is advised.lld:pubmed
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pubmed-article:10933881pubmed:authorpubmed-author:ChevionMMlld:pubmed
pubmed-article:10933881pubmed:authorpubmed-author:ZhuB ZBZlld:pubmed
pubmed-article:10933881pubmed:copyrightInfoCopyright 2000 Academic Press.lld:pubmed
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pubmed-article:10933881pubmed:articleTitleCopper-mediated toxicity of 2,4,5-trichlorophenol: biphasic effect of the copper(I)-specific chelator neocuproine.lld:pubmed
pubmed-article:10933881pubmed:affiliationDepartment of Cellular Biochemistry, Hebrew University-Hadassah Schools of Medicine and Dental Medicine, Jerusalem, 91120, Israel. benzhan.zhu@orst.edulld:pubmed
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