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Molecular mechanisms of Cr(VI)-induced carcinogenesis.

Authors
Ding-M; Shi-X
Source
Mol Cell Biochem 2002 May-Jun; 234-235(1-2):293-300
NIOSHTIC No.
20022164
Abstract
Although Cr(VI)-containing compounds are well documented carcinogens, their mechanism of action is still not well understood. Recent studies have suggested that reduction of Cr(VI) to its lower oxidation states and related free radical reactions play an important role in Cr(VI)-induced carcinogenesis. This article summarizes recent studies from our laboratory on (a) the reduction of Cr(VI) by ascorbate, diol- and thiol-containing molecules, certain flavoenzymes, cell organelles, intact cells, and whole animals; (b) free radical production in both non-cellular and cellular systems; and (c) Cr(VI)-induced DNA damage, activation of nuclear transcription factor KB (NF-kappaB), activator protein-1, p53, hypoxia-inducible factor-1, vascular endothelial growth factor, tyrosine phosphorylation, apoptosis, cell growth arrest, and gene expression profile.
Keywords
Chromium-compounds; Cancer; Carcinogenesis; Carcinogens; Cell-alteration; Cell-biology; Cell-growth; Laboratory-testing; Molecular-biology; Molecular-structure; Free-radicals; Oxidation-reduction-reactions; DNA-damage; Antioxidants; Enzymatic-effects; Enzyme-activity; Oxidative-enzymes; Genes
Contact
Pathology and Physiology Research Branch, Health Effects Laboratory Division, National Institute for Occupational Safety and Health, 1095 Willowdale Road, Morgantown, WV 26505, USA
CODEN
MCBIB8
Publication Date
20020501
Document Type
Journal Article
Email Address
xshi@cdc.gov
Fiscal Year
2002
NTIS Accession No.
NTIS Price
Issue of Publication
1-2
ISSN
0300-8177
NIOSH Division
HELD
Priority Area
Research Tools and Approaches: Cancer Research Methods
Source Name
Molecular and Cellular Biochemistry
State
WV
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