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Induction of gene expression by environmental oxidants associated with inflammation, fibrogenesis, and carcinogenesis.

Authors
Janssen-YM; Timblin-CR; Zanella-CL; Jimenez-LA; Mossman-BT
Source
Oxidative Stress and Signal Transduction 1996:387-414
Link
NIOSHTIC No.
00241818
Abstract
Induction of gene expression by mineral dusts and other oxidants capable of inducing inflammatory, fibrogenic, and carcinogenic responses was reviewed. The review described the characteristics of genes that play important roles in cell proliferation and discussed stress response genes, genes important in inducing inflammatory responses, cellular defense mechanisms against environmental agents that induce oxidative stress, gene expression involved in apoptosis, and considered signal transduction pathways involved in the induction of inflammatory processes by mineral dusts. A number of experimental studies have shown that mineral dusts such as asbestos (1332214) and crystalline silica (14808607) induce oxidative stress through inflammatory processes involving the cooperative action of various cytokines and chemokines. Signals generated extracellularly at the cell surface by these agents or by oxidants acting as second messengers can proceed along various pathways to induce a change in the phosphorylation status of transcription factors. This may then activate or inactivate transcription factors that will induce changes in gene expression that will culminate in endpoints such as apoptosis, fibrogenesis, or carcinogenesis. A nuclear transcription factor kappa B (NF-kappaB) dependent pathway appears to be the major mechanism underlying the inflammatory response that is observed in asbestos and crystalline silica induced pulmonary disease. NF-kappaB is a transcription factor involved in activation of genes that are involved in cell proliferation and inflammation. Many genes have NF- kappaB sites in their promoter regions that can be involved in gene expression.
Keywords
NIOSH-Grant; Pulmonary-system-disorders; Cancer; Mineral-dusts; Oxidative-processes; Physiological-stress; Cell-function; Genetics; Cell-division; Fibrogenicity; Respiratory-system-disorders
Contact
Pathology University of Vermont Medical Alumni Bldg Burlington, VT 05405
CAS No.
1332-21-4; 14808-60-7;
Publication Date
19960101
Document Type
Book or book chapter
Editors
Cadenas-E; Forman-HJ
Funding Amount
162000
Funding Type
Grant
Fiscal Year
1996
NTIS Accession No.
NTIS Price
Identifying No.
Grant-Number-K01-OH-000146
ISSN
041207681
Priority Area
Respiratory-system-disorders
Source Name
Oxidative Stress and Signal Transduction
State
NY; VT
Performing Organization
University of Vermont & St Agric College, Burlington, Vermont
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