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Activation of activator protein-1 by reactive oxygen species associated with asbestos.

Authors
Vallyathan-V; Ding-M; Shi-X; Castranova-V
Source
Toxicologist 2000 Mar; 54(1):254
NIOSHTIC No.
20021084
Abstract
Inhalation of asbestos causes alterations in cell signaling cascades, gene expression, cell injury and cell proliferation which may lead to pulmonary fibrosis, lung cancer, or mesothelioma. Asbestos-mediated free radical reactions are believed to trigger a number of cellular and molecular events that may promote fibrogenesis and carcinogenesis. Because activator protein I (AP-1) plays an important role in pre-neoplastic-to-neoplastic transformation tumor promotion and metastatsis, we studied the possible activation of AP-1 in vitro in cultured JB6 cells and in vivo using transgenic mice after exposure to crocidolite asbestos caused a significant (22-fold) activation of AP-1 in bronchiolar tissue compared to a moderate 10-fold increase in the lung tissue. The induction of AP-1 in asbestos exposure appears to be mediated through the phosphorylation of mitogen-activated protein kinases, Erk 1 and Erk 2. Hydroxyl radical scavengers inhibited asbestos-induced AP-1 activation. These data support the hypothesis that oxygen radical mechanisms may be associated with pulmonary fibrosis and carcinogenesis.
Keywords
Asbestosis; Asbestos-dust; Inhalation-studies; Pulmonary-system-disorders; Fibrosis; Lung-cancer; Respiratory-system-disorders; Free-radicals; Fibrogenesis; Fibrogenicity; Carcinogenesis; Carcinogenicity; Carcinogens; In-vitro-studies; In-vivo-studies; Laboratory-animals; Animals; Animal-studies
Publication Date
20000301
Document Type
Abstract
Fiscal Year
2000
NTIS Accession No.
NTIS Price
Issue of Publication
1
ISSN
1096-6080
NIOSH Division
HELD
Source Name
The Toxicologist. Society of Toxicology 39th Annual Meeting, March 19-23, 2000, Philadelphia, Pennsylvania
State
WV
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