Pro-inflammatory activity in rats of thiocyanate, a metabolite of the hydrocyanic acid inhaled from tobacco smoke

Whitehouse, Michael Wellesley and Jones, Mark (2009) Pro-inflammatory activity in rats of thiocyanate, a metabolite of the hydrocyanic acid inhaled from tobacco smoke. Inflammation Research, 58 10: 693-704. doi:10.1007/s00011-009-0038-2


Author Whitehouse, Michael Wellesley
Jones, Mark
Title Pro-inflammatory activity in rats of thiocyanate, a metabolite of the hydrocyanic acid inhaled from tobacco smoke
Journal name Inflammation Research   Check publisher's open access policy
ISSN 1023-3830
1420-908X
Publication date 2009-10
Sub-type Article (original research)
DOI 10.1007/s00011-009-0038-2
Volume 58
Issue 10
Start page 693
End page 704
Total pages 12
Editor Michael J. Parnham
Place of publication Basel, Switzerland
Publisher Birkhaeuser Verlag
Collection year 2010
Language eng
Formatted abstract
Objective To seek a mechanism linking tobacco smoking with the increased incidence and severity of rheumatoid arthritis, deduced from many retrospective surveys, by studying arthritis/fibrosis development in rats.

Methods Rats ([300) received low levels of sodium/potassium thiocyanate (10 or 25 mmol/l) in their drinking water to raise their blood thiocyanate levels, mimicking the elevated levels of blood, salivary and urinary thiocyanate found in smokers.

Results Thiocyanate supplements increased the severity of experimental arthritis induced by tailbase injection of (1) Freund’s complete adjuvants (mycobacteria plus various adjuvant-active oils), (2) collagen type-II with Freund’s incomplete adjuvant (no mycobacteria), (3) the synthetic lipid amine, avridine in an oil and (4) the natural hydrocarbons squalene (C30H50) and pristane (C19H40). This proarthritic effect was independent of sex, rat strain or changing diet and housing facilities. Thiocyanate supplements also amplified the acute/persisting inflammatory responses to paw injections of pristane, zymosan and microcrystalline hydroxyapatite. Iodide salts also mimicked some of these effects of thiocyanate.

Conclusion Thiocyanate, a detoxication product of HCN present in tobacco smoke, increased (or even induced) inflammatory responses to several agents causing arthritis or fibrotic inflammation in rats. It, therefore, can act as a co-arthritigen, or ‘virulence factor’ and could be a therapeutic target to reduce arthritis expression and morbidity.
Keyword Tobacco smoke
Hydrocyanic acid/cyanide
Thiocyanate
Experimental rat arthritis
Hydroxyapatite
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ

 
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Created: Thu, 08 Apr 2010, 11:41:24 EST by Fiona Mactaggart on behalf of Medicine - Princess Alexandra Hospital