TY - JOUR
T1 - Reactive oxygen species and molecular mechanism of silica-induced lung injury
AU - Shi, X.
AU - Ding, M.
AU - Chen, F.
AU - Wang, L.
AU - Rojanasakul, Y.
AU - Vallyathan, V.
AU - Castranova, V.
PY - 2001
Y1 - 2001
N2 - 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 silicastimulated cells. This article also discusses the role of ROS in silica-induced lung injury, with particular focus on the silica-induced NF-κB activation, including the molecular mechanisms of its regulation, its possible attenuation, and its relationship to silica-induced generation of cyclooxygenase II and TNF-α.
AB - 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 silicastimulated cells. This article also discusses the role of ROS in silica-induced lung injury, with particular focus on the silica-induced NF-κB activation, including the molecular mechanisms of its regulation, its possible attenuation, and its relationship to silica-induced generation of cyclooxygenase II and TNF-α.
KW - Cyclooxygenase II
KW - Free radicals
KW - NF-κB
KW - Reactive oxygen species
KW - Silicosis
KW - TNF-α
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U2 - 10.1615/jenvironpatholtoxicoloncol.v20.isuppl.1.80
DO - 10.1615/jenvironpatholtoxicoloncol.v20.isuppl.1.80
M3 - Article
C2 - 11570677
AN - SCOPUS:0034838112
SN - 0731-8898
VL - 20
SP - 85
EP - 93
JO - Journal of Environmental Pathology, Toxicology and Oncology
JF - Journal of Environmental Pathology, Toxicology and Oncology
IS - SUPPL. 1
ER -