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  • Role of oxidative stress, mitochondrial membrane potential, and calcium homeostasis in nickel subsulfide-induced human lymphocyte death in vitro.

Role of oxidative stress, mitochondrial membrane potential, and calcium homeostasis in nickel subsulfide-induced human lymphocyte death in vitro.

The Science of the total environment (2006-06-20)
Prosper M'Bemba-Meka, Nicole Lemieux, Saroj K Chakrabarti
要旨

When isolated human lymphocytes were treated in vitro either with various concentrations (0-2 mM) of soluble form of nickel subsulfide (Ni3S2) at 37 degrees 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.

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ブランド
製品内容

Sigma-Aldrich
硫化ニッケル, 99.7% trace metals basis, −150 mesh