کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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4433934 | 1619966 | 2006 | 14 صفحه PDF | دانلود رایگان |

When isolated human lymphocytes were treated in vitro either with various concentrations (0–2 mM) of soluble form of nickel subsulfide (Ni3S2) at 37 °C for 4 h or at various times (0–240 min), both concentration- and time-dependent effects of Ni3S2 on lymphocyte death were observed. Increased generation of hydrogen peroxide (H2O2), and superoxide anion (O2−), lipid peroxidation and depletion of both nonprotein (NP-) and protein (P-) sulfhydryl (SH) contents were induced by 1 mM Ni3S2. Ni3S2-induced lymphocyte death was significantly prevented by pre-treatment with either catalase (a H2O2 scavenger), or superoxide dismutase (scavenger of O2− 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 Ni3S2-induced disturbances in mitochondrial membrane potential, and significantly prevented Ni3S2-induced lymphocyte death. Ni3S2-induced lymphocyte death was also significantly prevented by modulating intracellular calcium fluxes using both Ca2+ channel blockers and intracellular Ca2+ antagonists. Thus, the mechanism of soluble Ni3S2-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.
Journal: Science of The Total Environment - Volume 369, Issues 1–3, 1 October 2006, Pages 21–34