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 Hartwig, A
Right arrow Articles by Hartmann, M
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Hartwig, A
Right arrow Articles by Hartmann, M
Annals of Clinical and Laboratory Science, Vol 26, Issue 1, 31-38
Copyright © 1996 by Association of Clinical Scientists


Articles

Interaction of carcinogenic metal compounds with deoxyribonucleic acid repair processes

A Hartwig, R Schlepegrell, H Dally, and M Hartmann

The potentials of nickel(II) and cadmium(II) to interfere with the repair of different types of deoxyribonucleic acid (DNA) lesions was investigated. Concerning the nucleotide excision repair pathway, nickel(II) has been shown to reduce the incision and the ligation frequency after ultraviolet (UV)-irradiation. When applying a gel mobility shift assay and HeLa nuclear cell free extracts, nickel(II) diminishes the specific binding of a protein to UV-damaged DNA, suggesting that nickel(II) interferes with the DNA-protein interactions involved in the damage recognition after UV-irradiation. Similarly, the incision frequency is reduced in the presence of low concentrations of cadmium(II). Concerning the repair of oxidative DNA damage induced by visible light, non-cytotoxic concentrations of nickel(II) caused a complete repair inhibition of DNA base modifications like 7,8-dihydro-8-oxoguanine (8-hydroxyguanine) and of DNA strand breaks. Since the repair of DNA damage is essential for the prevention of cancer, its inhibition may account for the carcinogenic action of the respective metal compounds.


This article has been cited by other articles:


Home page
Toxicol SciHome page
Y. Knobel, M. Glei, A. Weise, K. Osswald, A. Schaferhenrich, K. K. Richter, U. Claussen, and B. L. Pool-Zobel
Uranyl Nitrilotriacetate, a Stabilized Salt of Uranium, is Genotoxic in Nontransformed Human Colon Cells and in the Human Colon Adenoma Cell Line LT97
Toxicol. Sci., October 1, 2006; 93(2): 286 - 297.
[Abstract] [Full Text] [PDF]


Home page
CarcinogenesisHome page
W. Hu, Z. Feng, and M.-s. Tang
Nickel (II) enhances benzo[a]pyrene diol epoxide-induced mutagenesis through inhibition of nucleotide excision repair in human cells: a possible mechanism for nickel (II)-induced carcinogenesis
Carcinogenesis, March 1, 2004; 25(3): 455 - 462.
[Abstract] [Full Text] [PDF]




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