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Silica binding and toxicity in alveolar macrophages

Posted Dec 08 2009 12:00am

By Raymond F and Colleague

Inhalation of the crystalline form of silica is associated with a variety of pathologies from acute lung inflammation to silicosis, in addition to autoimmune disorders and cancer.

Basic science researchers looking at the mechanisms involved with the earliest initiators of disease are focused on how the alveolar macrophage (AM) interacts with the inhaled silica particle and the consequences of silica-induced toxicity on the cellular level. Based on experimental results, several rationales have been developed on exactly how crystalline silica particles are toxic to the macrophage cell that is functionally responsible for clearance of the foreign particle.

For example, silica is capable of producing reactive oxygen species (ROS) either directly (on the particle surface) or indirectly (produced by the cell as a response to silica) triggering cell-signaling pathways initiating cytokine release and apoptosis. With murine macrophages, reactive nitrogen species (RNS) are produced in the initial respiratory burst in addition to ROS.

An alternative explanation for silica toxicity includes lysosomal permeability, where silica disrupts the normal internalization process leading to cytokine release and cell death. Still other research has focused on the cell surface receptors (collectively known as scavenger receptors) involved in silica binding and internalization. The silica-induced cytokine release and apoptosis is described as the function of receptor-mediated signaling rather than free radical damage. Current research ideas on silica toxicity and binding in the alveolar macrophage are reviewed and discussed.

Silicon (Si) is the second most abundant element on earth next to carbon. A Si atom combined with 2 oxygen (O) atoms creates silicon oxide or silica (SiO2) naturally occurring as quartz or sand. There are multiple crystalline forms and one amorphous form of silica. Inhalation of the crystalline form of silica has been historically associated with the development of a severe respiratory disease, silicosis, which is a lung pneumoconiosis characterized by alveolar proteinosis and diffuse fibrosis resulting in progressively restrictive lung function.

Silicosis has been primarily associated with long occupational exposures to crystalline silica that typically occur in sandblasting, silica milling, rock drilling and tunneling. There is evidence that silica exposure can also be linked to the development of autoimmune diseases such as scleroderma (systemic sclerosis), rheumatoid arthritis, chronic renal disease and lupus.

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