| Literature DB >> 11811922 |
Min Ding1, Fei Chen, Xianglin Shi, Berran Yucesoy, Brooke Mossman, Val Vallyathan.
Abstract
While silica particles are considered to be fibrogenic and carcinogenic agents, the mechanisms responsible are not well understood. This article summarizes literature on silica-induced accelerated silicosis, chronic silicosis, silico-tuberculosis, bronchogenic carcinoma, and immune-mediated diseases. This article also discusses the generation of reactive oxygen species (ROS) that occurs directly from the interaction of silica with aqueous medium and from silica-stimulated cells, the molecular mechanisms of silica-induced lung injuries with focus on silica-induced NF-kappaB activation, including its mechanisms, possible attenuation and relationship to silica-induced generation of cyclooxygenase II and TNF-alpha. Silica-induced AP-1 activation, protooncogene expression, and the role of ROS in these processes are also briefly discussed.Entities:
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Year: 2002 PMID: 11811922 DOI: 10.1016/s1567-5769(01)00170-9
Source DB: PubMed Journal: Int Immunopharmacol ISSN: 1567-5769 Impact factor: 4.932