Abstract
Silica particles are considered to be fibrogenic and carcinogenic agents, but the mechanisms of disease initiation and progression are not fully understood. This article summarizes the literature on the generation of reactive oxygen species (ROS) directly from interaction of silica with aqueous medium and from silica-stimulated cells. This article also discusses the role of ROS in silica-induced lung injury, with particular focus on the silica-induced NF-kappaB activation, including the molecular mechanisms of its regulation, its possible attenuation, and its relationship to silica-induced generation of cyclooxygenase II and TNF-alpha.
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