Nickel hydroxy carbonate increases tumour necrosis factor alpha and interleukin 6 secretion by alveolar macrophages

J Appl Toxicol. 1994 Sep-Oct;14(5):375-9. doi: 10.1002/jat.2550140510.

Abstract

The aim of the current study was to assess the in vitro effects of nickel hydroxy carbonate (NiHC) at noncytotoxic concentrations on the production of cytokines such as tumour necrosis factor alpha (TNF-alpha) and interleukin 6 (IL-6) in alveolar macrophages (AMs). The effect of NiHC was evaluated in both unstimulated AMs and cells activated by lipopolysaccharide (LPS). Cytotoxicity was related to lactate dehydrogenase release and ATP cell content. The results confirm that NiHC at concentrations of 0.125, 1.25 and 3.125 micrograms NiHC 10(-6) cells was not cytotoxic. The NiHC exposure of unstimulated AMs significantly increased the release of TNF-alpha at all concentrations and that of IL-6 at 1.25 micrograms NiHC 10(-6) cells. LPS addition significantly increased the secretion of both cytokines. However, NiHC did not cause a significant increase in the release of TNF-alpha and IL-6 in LPS-stimulated cells. In conclusion, the ability of NiHC to activate AMs and to release increased amounts of pro-inflammatory mediators may be responsible, at least partly, for inflammation and pneumotoxicity associated with nickel exposure.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenosine Triphosphate / metabolism
  • Animals
  • Carbonates / toxicity*
  • Cells, Cultured
  • Guinea Pigs
  • Interleukin-6 / biosynthesis*
  • L-Lactate Dehydrogenase / metabolism
  • Macrophages, Alveolar / drug effects*
  • Macrophages, Alveolar / immunology
  • Nickel / toxicity*
  • Tumor Necrosis Factor-alpha / biosynthesis*

Substances

  • Carbonates
  • Interleukin-6
  • Tumor Necrosis Factor-alpha
  • nickel hydroxycarbonate
  • Nickel
  • Adenosine Triphosphate
  • L-Lactate Dehydrogenase