ACLS
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Luo, H
Right arrow Articles by Dalal, N.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Luo, H
Right arrow Articles by Dalal, N.
Annals of Clinical and Laboratory Science, Vol 26, Issue 2, 185-191
Copyright © 1996 by Association of Clinical Scientists

Articles

Chromium (IV)-mediated fenton-like reaction causes DNA damage: implication to genotoxicity of chromate

H Luo, Y Lu, X Shi, Y Mao, and NS Dalal

This paper describes our deoxyribonucleic acid (DNA) damage and Fenton activity studies on Cr(IV) that were undertaken to examine a role of Cr(IV) in the biochemical mechanism of genotoxicity of Cr(VI) compounds. A Cr(IV)-containing compound, a Cr(IV)-ester, was synthesized and used as the first model compound for Cr(IV) studies. Electron spin resonance measurements demonstrated that in the presence of H2O2, this Cr(IV) compound acts as a potent Fenton-like reagent, i.e., it generates OH radical and a Cr(V) species (g = 1.9787) via: Cr(IV) + H2O2-->Cr(V) + OH + OH-. Measurements of OH yield as a function of H2O2 concentration showed that Cr(IV) is more potent than Cr(V) in generating OH. DNA damage assays demonstrate that Cr(IV) and the Cr(IV)/H2O2-generated OH radical can cause DNA strand breaks. The DNA damage caused by OH radical can be effectively blocked by OH radical scavengers. These results thus constitute the first direct evidence for DNA damage by Cr(IV) and Cr(IV)-mediated Fenton-like reaction and support the conjecture that Cr(IV) plays a significant role in the biochemical mechanism of the genotoxic reactions of Cr(VI) compounds and that this effect can be modulated by suitable antiradical agents.


This article has been cited by other articles:


Home page
 CarcinogenesisHome page
N. Azad, A. K. V. Iyer, A. Manosroi, L. Wang, and Y. Rojanasakul
Superoxide-mediated proteasomal degradation of Bcl-2 determines cell susceptibility to Cr(VI)-induced apoptosis
Carcinogenesis, August 1, 2008; 29(8): 1538 - 1545.
[Abstract] [Full Text] [PDF]

Home page
 Mol. Cell. ProteomicsHome page
S. D. Brown, M. R. Thompson, N. C. VerBerkmoes, K. Chourey, M. Shah, J. Zhou, R. L. Hettich, and D. K. Thompson
Molecular Dynamics of the Shewanella oneidensis Response to Chromate Stress
Mol. Cell. Proteomics, June 1, 2006; 5(6): 1054 - 1071.
[Abstract] [Full Text] [PDF]

Home page
 MicrobiologyHome page
E. R. Sumner, A. Shanmuganathan, T. C. Sideri, S. A. Willetts, J. E. Houghton, and S. V. Avery
Oxidative protein damage causes chromium toxicity in yeast
Microbiology, June 1, 2005; 151(6): 1939 - 1948.
[Abstract] [Full Text] [PDF]

Home page
 MutagenesisHome page
G. Speit and I. Bonzheim
Genotoxic and protective effects of hyperbaric oxygen in A549 lung cells
Mutagenesis, November 1, 2003; 18(6): 545 - 548.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1996 by the Association of Clinical Scientists.