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

doi:10.1006/taap.2001.9268

Toxicology and Applied Pharmacology

Volume 176, Issue 1, 1 October 2001, Pages 10-17

https://doi.org/10.1006/taap.2001.9268 Get rights and content

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.

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No ROS generation was observed in DQ12-exposed J774A.1 cells, where the level remained constant, irrespective of time and concentration studied. This result was highly unexpected as it has been shown that crystalline silica can induce on its surface, formation of silicon-based free radicals, which in aqueous suspensions generate ROS, including H2O2, ·OH and O2•¯ (Fubini and Hubbard, 2003; Shi et al., 1998; Donaldson and Borm, 1998; Duffin et al., 2001). Moreover, crystalline silica is a potent stimulant of the respiratory burst in phagocytic cells which leads to ROS/RNS production (Zhang et al., 2010; van Berlo et al., 2010).
Natural Layered Silicates (NLS) and Synthetic Layered Silicates (SLS) are a diverse group of clay minerals that have attracted great interest in various branches of industry. However, despite growing demand for this class of material, their impact on human health has not been fully investigated. Therefore, the aim of this study was to evaluate and compare the potential toxic effects of a wide range of commercially available SLS and NLS of varying physicochemical properties (lithium (Li) or fluoride (F) content and size). Mouse BALB/c monocyte macrophage (J774A.1) and human monocyte-derived macrophages (MDMs) were chosen as in vitro models of alveolar macrophages.
Montmorillonite, hectorite, Medium (med) F/High Li and Low F/Med Li particles, were cytotoxic to cells and induced potent pro-inflammatory responses. The remaining particles (No F/Very (V)Low Li, No F/Med Li, No F/Low Li, High F/Med Li and High F/Med Li washed) were non- to relatively low- cytotoxic and inflammogenic, in both type of cells. In an acellular condition none of the tested samples increased reactive oxygen species (ROS), while ROS generation was observed following exposure to sublethal concentrations of Med F/High Li, Low F/Med Li, montmorillonite and hectorite samples, in J774A.1 cells.
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Citation Excerpt :
Elements incorporated structurally will be present at the surface of the particle, as well as internally. Al treatment of the quartz surface decreases its cytotoxic potency, ability to induce inflammatory indicators, and its haemolytic potency (Duffin et al., 2001; Nolan et al., 1981). It has been suggested that an Al treatment would bind to silanols (a surface functional group with the connectivity Si–O–H) on the silica surface, replacing H+ and, thereby, prevent the adsorption of cell membrane components to the silica surface (Fubini, 1998).
Exposure to crystalline silica (SiO₂), in the form of quartz, tridymite or cristobalite, can cause respiratory diseases, such as silicosis. However, the observed toxicity and pathogenicity of crystalline silica is highly variable. This has been attributed to a number of inherent and external factors, including the presence of impurities. In cristobalite-rich dusts, substitutions of aluminium (Al) for silicon (Si) in the cristobalite structure, and impurities occluding the silica surface, have been hypothesised to decrease its toxicity. This hypothesis is tested here through the characterisation and in vitro toxicological study of synthesised cristobalite with incremental amounts of Al and sodium (Na) dopants.
Samples of synthetic cristobalite with incremental amounts of Al and Na impurities, and tridymite, were produced through heating of a silica sol-gel. Samples were characterised for mineralogy, cristobalite purity and abundance, particle size, surface area and surface charge. In vitro assays assessed the ability of the samples to induce cytotoxicity and TNF-α production in J774 macrophages, and haemolysis of red blood cells.
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Regular ArticleAluminium Lactate Treatment of DQ12 Quartz Inhibits Its Ability to Cause Inflammation, Chemokine Expression, and Nuclear Factor-κB Activation

Abstract

Toxicol. Appl. Pharmacol.

Ann. Occup. Hyg.

Ann. Occup. Hyg.

Ann. Occup. Hyg.

Environ. Res.

J. Biol. Chem.

Biochem. Biophys. Res. Commun.

Ann. Occup. Hyg.

Toxicol. Appl. Pharmacol.

Effect of short-term exogenous pulmonary surfactant treatment on acute lung damage associated with the intratracheal instillation of silica

J. Toxicol. Environ. Health

Aluminium lactate treatment alters the lung biological activity of quartz

Exp. Lung Res.

Augmentation of pulmonary reactions to quartz inhalation by trace amounts of iron-containing particles

Environ. Health Perspect.

Inflammatory effects of respirable quartz collected in workplaces versus standard DQ12 quartz: particle surface correlates

Toxicol. Sci.

Cytokines and particle-induced inflammatory cell recruitment

Environ. Health Perspect.

Characterizing mutagenesis in the hprt gene of rat alveolar epithelial cells

Exp. Lung Res.

Macrophage inflammatory proteins 1 and 2: Expression by rat alveolar macrophages, fibroblasts, and epithelial cells and in rat lung after mineral dust exposure 1

Am. J. Respir. Cell Mol. Biol.

Alpha-quartz-induced chemokine expression by rat lung epithelial cells: Effects of in vivo and in vitro particle exposure

Am. J. Pathol.

Health effects of silica

Chemical functionalities at the silica surface determining its reactivity when inhaled. Formation and reactivity of surface radicals

Toxicol. Ind. Health

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