Skip directly to search Skip directly to A to Z list Skip directly to page options Skip directly to site content

NIOSHTIC-2 Publications Search

Search Results

Reactive oxygen species and molecular mechanism of silica-induced lung injury.

Authors
Shi-X; Ding-M; Chen-F; Wang-L; Rojanasakul-Y; Vallyathan-V; Castranova-V
Source
J Environ Pathol Toxicol Oncol 2001 Jan; 20(Suppl 1):85-93
NIOSHTIC No.
20021871
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.
Keywords
Silicosis; Carcinogens; Fibrogenicity; Diseases; Lung; Injuries; Author Keywords: silicosis; reacive oxygen species; free radicals; NF-kappaB; TNF-alpha; cyclooxygenase II
CODEN
JEPOEC
Publication Date
20010101
Document Type
Journal Article
Email Address
xas0@cdc.gov
Editors
Moran-EM
Fiscal Year
2001
NTIS Accession No.
NTIS Price
ISSN
0731-8898
NIOSH Division
HELD
Priority Area
Other Occupational Concerns; Pulmonary System Disorders
Source Name
Journal of Environmental Pathology, Toxicology, and Oncology
State
WV
TOP