title: [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.
authors.affiliation: Affiliated Hospital, Medical College, Chinese People's Armed Polices Forces, Tianjin 300162, China.
authors.forename: Haike
authors.initials: H
authors.lastname: Du
authors.forename: Shixin
authors.initials: S
authors.lastname: Wang
mesh_terms: D000818:Animals; D017563:Lung Diseases, Interstitial / Q000378:metabolism; D051379:Mice; D016328:NF-kappa B / Q000378:metabolism; D009569:Nitric Oxide / Q000096:biosynthesis*; D011658:Pulmonary Fibrosis / Q000378:metabolism; D051381:Rats; D012829:Silicosis / Q000378:metabolism* / Q000473:pathology; D013997:Time Factors
chemical_list: D016328:NF-kappa B; D009569:Nitric Oxide