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- Published by: Elsevier October 1, 2006
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This digital document is a journal article from Science of the Total Environment, The, published by Elsevier in 2006. The article is delivered in HTML format and is available in your Amazon.com Media Library immediately after purchase. You can view it with any web browser.
Description: When isolated human lymphocytes were treated in vitro either with various concentrations (0-2 mM) of soluble form of nickel subsulfide (Ni"3S"2) at 37 ^oC for 4 h or at various times (0-240 min), both concentration- and time-dependent effects of Ni"3S"2 on lymphocyte death were observed. Increased generation of hydrogen peroxide (H"2O"2), and superoxide anion (O"2^-), lipid peroxidation and depletion of both nonprotein (NP-) and protein (P-) sulfhydryl (SH) contents were induced by 1 mM Ni"3S"2. Ni"3S"2-induced lymphocyte death was significantly prevented by pre-treatment with either catalase (a H"2O"2 scavenger), or superoxide dismutase (scavenger of O"2^- radical), or dimethylthiourea/mannitol (hydroxyl radical scavengers), or deferoxamine (iron-chelator), or glutathione/N-acetylcysteine. Co-treatment with cyclosporin A (a mitochondrial membrane potential' inhibitor) inhibited Ni"3S"2-induced disturbances in mitochondrial membrane potential, and significantly prevented Ni"3S"2-induced lymphocyte death. Ni"3S"2-induced lymphocyte death was also significantly prevented by modulating intracellular calcium fluxes using both Ca^2^+ channel blockers and intracellular Ca^2^+ antagonists. Thus, the mechanism of soluble Ni"3S"2-induced activation of lymphocyte death signalling pathways involves increasing generation of different types of oxidative stress, disturbances in mitochondrial membrane potential and cellular calcium homeostasis' destabilization.
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