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 silica-induced carcinogenesis.

Authors
Shi-X; Castranova-V; Halliwell-B; Vallyathan-V
Source
J Toxicol Environ Health, B 1998 Jul-Sep; 1(3):181-197
NIOSHTIC No.
20025048
Abstract
Although silica has recently been designated as a carcinogen, its mechanism of carcinogenesis is not fully understood. Recent studies suggest that free-radical reactions may play an important role in the initiation and progression of cancer. This article summarizes literature on the generation of reactive oxygen species (ROS) directly from silica and from silica-stimulated cells. It also summarizes information concerning the role of ROS in silica-induced DNA damage as well as in silica-induced cell proliferation, including the effects of silica on the activation of nuclear transcription factors, induction of growth factors and oncogene expression, redox regulation of the p53 tumor suppressor gene, induction of apoptosis, and division of damaged cells. Understanding the role of ROS in silica-mediated reactions may help develop therapeutic agents to block silica-induced free radical reactions and thus prevent or attenuate silica-induced carcinogenesis.
Keywords
Silicates; Silica-dusts; Silicosis; Carcinogens; Carcinogenicity; Cancer; Free-radicals; Cell-damage; Cellular-function; Cellular-reactions; Cellular-structures
Contact
Xianglin Shi, PhD, Pathology and Physiology Research Branch, NIOSH, 1095 Willowdale Road, Morgantown, WV 26505, USA
CODEN
JTECFR
Publication Date
19980701
Document Type
Journal Article
Email Address
xas0@cdc.gov
Fiscal Year
1998
NTIS Accession No.
NTIS Price
Issue of Publication
3
ISSN
1093-7404
NIOSH Division
HELD
Source Name
Journal of Toxicology and Environmental Health, Part B: Critical Reviews
State
WV
TOP