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Nickel(II)-induced apoptosis in murine T cell hybridoma cells is associated with increased Fas ligand expression

  1. Author:
    Kim, K.
    Lee, S. H.
    Seo, Y. R.
    Perkins, S. N.
    Kasprzak, K. S.

  2. Author Address

    NCI, Basic Res Lab, Ctr Canc Res, Bldg 538,Room 205-E, Frederick, MD 21701 USA NCI, Basic Res Lab, Ctr Canc Res, Frederick, MD 21701 USA NCI, Comparat Carcinogenesis Lab, Ctr Canc Res, Frederick, MD 21701 USA Korea Univ, Grad Sch Biotechnol, Cell Biol Lab, Seoul 136701, South Korea NCI, Off Prevent Oncol, Div Canc Prevent, Ctr Canc Res, Bethesda, MD 20892 USA NCI, Lab Biosyst & Canc, Ctr Canc Res, Bethesda, MD 20892 USA Perkins SN NCI, Basic Res Lab, Ctr Canc Res, Bldg 538,Room 205-E, Frederick, MD 21701 USA
    1. Year: 2002
  2. Journal: Toxicology and Applied Pharmacology
    1. 185
    2. 1
    3. Pages: 41-47
  4. Type of Article: Article
  1. Abstract:

    Nickel(II) exposure has multiple effects on the immune system, including thymic involution, decreased T cell number in the spleen, and decreased natural killer cell activity. Using a murine T cell hybridoma cell line (KMIs 8.3.5.1) to model nickel-induced cell death in immune cells, we found that nickel(II) acetate treatment rapidly induced apoptosis in these cells, as signified by membrane blebbing, chromatin condensation, increased annexin V staining, and an increased proportion of cells with hypodiploid DNA. Preceding these morphological changes, nickel(II) treatment increased expression of Fas ligand (FasL) mRNA and protein levels and also increased caspase-3-like protease activity. Coincubation with caspase inhibitors markedly inhibited nickel(II)-induced apoptosis, with Z-IETD-FMK, an inhibitor of caspase-8 and granzyme B, nearly as, effective as less selective caspase inhibitors. Agents that generate reactive oxygen species (ROS) cause apoptosis in a variety of cells by inducing expression of FasL. Given that nickel(II) can directly generate ROS, exposure to nickel(II) may lead to apoptosis through a similar mechanism. (C) 2002 Elsevier Science (USA).

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