[Nitric oxide and early inflammatory injury in silicosis]

Abstract

There is a body of evidence that NO formation could be implicated in mediating silica-induced pulmonary fibrosis. As a reactive free radical, NO may not only contribute to lung parenchymal tissue injury but also has the ability to combine with superoxide and form a highly reactive toxic species-peroxynitrite, which can induce extensive cellular toxicity via a variety of mechanisms in the lung tissues. Several cytokine is required for NO production. NF-kappa B plays a particularly important role in the regulation of gene expression of the iNOS isoform. There are discrepancy between the current literature regarding the role NO in the NF-kappa B activation and therefore, in this paper, the role of NO in the cellular and molecular mechanisms of silica-induced lung damage was reviewed.