In-vivo study of genotoxic and inflammatory effects of the organo-modified Montmorillonite Cloisite® 30B

• Published in: Mutation research. Genetic toxicology and environmental mutagenesis 2014-08, Vol.770, p.66-71
• Main Authors: Sharma, A.K., Mortensen, A., Schmidt, B., Frandsen, H., Hadrup, N., Larsen, E.H., Binderup, M.-L.
• Format: Article
• Language: English
• Subjects: Absorption; Aluminum Silicates - toxicity; Animals; Bentonite - toxicity; Biomarkers - blood; Chromatography; Clay; Colon - cytology; Colon - drug effects; Colon - metabolism; Comet Assay; Cytokines - blood; Deoxyribonucleic acid; DNA; DNA Damage - drug effects; Dose-Response Relationship, Drug; Effects; Female; Genetics; Inflammation; Inflammation - chemically induced; Inflammation - pathology; Kidney - cytology; Kidney - drug effects; Kidney - metabolism; Liver - cytology; Liver - drug effects; Liver - metabolism; Male; Mass spectrometry; Nanocomposite; Quaternary ammonium compound; Quaternary Ammonium Compounds - toxicity; Rats; Rats, Wistar; Toxicity
• ISSN: 1383-5718; 1879-3592
• DOI: 10.1016/j.mrgentox.2014.04.023

•Cloisite® 30B was tested for DNA-damage induction in rats with the alkaline version of the comet assay. No DNA strand-breaks were observed in liver, kidney and colon cells.•The inflammatory potential was investigated in rat blood-plasma samples and no induction of inflammatory cytokine markers was observed.•ICP-MS was performed of liver, kidney and faeces samples with aluminium as a tracer element. There was no indication of systemic exposure to clay particles from Cloisite® 30B.•HPLC-Q-TOF/MS analysis detected quaternary ammonium analogues in the top dose, corresponding to an exposure of rats about 5mg quaternary ammonium analogues/kg body weight. Because of the increasing use of clays and organoclays in industrial applications it is of importance to consider the toxicity of these materials. Recently it was reported that the commercially available Montmorillonite clay, Cloisite® 30B, which is surface-modified by organic quaternary ammonium compounds, was genotoxic in vitro. In the present study the in-vivo genotoxic and inflammatory potential of Cloisite® 30B was investigated as a follow-up of the in-vitro studies. Wistar rats were exposed to Cloisite® 30B twice 24h apart by oral gavage, at doses ranging from 250 to 1000mg/kg body weight [indicate duration of treatment; Ed.]. There was no induction of DNA strand-breaks in colon, liver and kidney cells and there was no increase in inflammatory cytokine markers in blood-plasma samples. In order to verify the possible absorption of Cloisite® 30B from the gastrointestinal tract, inductively coupled plasma mass-spectrometry (ICP-MS) analysis was performed on samples of liver, kidney and faeces, with aluminium as a tracer element characteristic to clay. The results showed that aluminium could be detected in faeces, but not in the liver or kidneys. This indicated that there was no systemic exposure to clay particles from Cloisite® 30B. Detection and identification of free quaternary ammonium modifier in the highest dose of Cloisite® 30B was carried out by high-performance liquid chromatography coupled with quadrupole time-of-flight mass spectrometry (HPLC-Q-TOF-MS). This analysis revealed a mixture of three quaternary ammonium analogues. The detected concentration of the organomodifier corresponded to an exposure of rats to about 5mg quaternary ammonium analogues/kg body weight.