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Aluminium Lactate Treatment of DQ12 Quartz Inhibits Its Ability to Cause Inflammation, Chemokine Expression, and Nuclear Factor-κB Activation

Duffin, Rodger; Gilmour, Peter S.; Schins, Roel P.F.; Clouter, Anna; Guy, Keith; Brown, David M.; MacNee, William; Borm, Paul J.; Donaldson, Kenneth; Stone, Vicki

Authors

Rodger Duffin

Peter S. Gilmour

Roel P.F. Schins

Anna Clouter

Keith Guy

David M. Brown

William MacNee

Paul J. Borm

Kenneth Donaldson

Vicki Stone



Abstract

In 1997, an IARC Working Group classified quartz (crystalline silica) as a Group 1 lung carcinogen, but only in some industries, i.e., the quartz hazard is a variable entity. The reactivity of the quartz surface may underlie its ability to cause inflammation, and treatments that ameliorate this reactivity will reduce the quartz hazard. In this study we treated quartz (Q) with aluminium lactate (AL), a procedure that is reported to decrease the quartz hazard, and explored the effect this had on the highly reactive quartz surface and on proinflammatory events in rat lungs. Aluminium lactate-treated quartz showed a reduced surface reactivity as measured by electron spin resonance and the hemolysis assay. Eighteen hours after instillation of Q into the rat lung, there was massive inflammation as indicated by the number of neutrophils in the bronchoalveolar lavage (BAL). In addition, Q induced an increase in BAL macrophage inflammatory protein-2 (MIP-2) while ALQ had no significant effect compared to control. Epithelial damage, as indicated by BAL protein and gamma glutamyl transpeptidase, also increased with Q but not with ALQ. Furthermore, Q induced an increase in MIP-2 mRNA by BAL cells while ALQ had no effect compared to controls. There was an increase in nuclear binding of the transcription nuclear factor κB (NF-κB) in the Q-exposed BAL cells and again no effect on nuclear NF-κB binding in BAL cells from ALQ-exposed rats. In conclusion, treatment of the quartz surface with aluminium lactate reduced the reactivity of the particles both in terms of hydroxyl radical generation and in terms of the induction of molecular signaling events leading to inflammation.

Citation

Duffin, R., Gilmour, P. S., Schins, R. P., Clouter, A., Guy, K., Brown, D. M., MacNee, W., Borm, P. J., Donaldson, K., & Stone, V. (2001). Aluminium Lactate Treatment of DQ12 Quartz Inhibits Its Ability to Cause Inflammation, Chemokine Expression, and Nuclear Factor-κB Activation. Toxicology and Applied Pharmacology, 176(1), 10-17. https://doi.org/10.1006/taap.2001.9268

Journal Article Type Article
Publication Date 2001-10
Deposit Date Jun 3, 2008
Print ISSN 0041-008X
Electronic ISSN 1096-0333
Publisher Elsevier
Peer Reviewed Peer Reviewed
Volume 176
Issue 1
Pages 10-17
DOI https://doi.org/10.1006/taap.2001.9268
Keywords Quartz, Aluminium lactate, Inflammation, Macrophage inflammatory protein-2, Free radicals
Public URL http://researchrepository.napier.ac.uk/id/eprint/1624



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