- Wolf et al 1989 (done in prior post)
- Landon et al 2004
- Bacon et al 1983
- Martnett et al 1999
- Hartwig et al 2003
- Witkiewicz-Kucharczyk and Bal 2006
Metal induced intracellular effects:
In the two articles below, you will see that in cells, 2 main processes exist to correct DNA aberations. Under similation by Chromium 6 and Cobalt, both of these repair mechanisms are inhibited. So the metal causes the permanent damage in the DNA but the repair mechnisms that would typically remidy the situation, don't work.
Modulation of DNA repair processes by arsenic and selenium compounds.
SourceInstitut für Lebensmittelchemie und Toxikologie, Universität Karlsruhe, Postfach 6980, D-76128 Karlsruhe, Germany. firstname.lastname@example.org
AbstractNickel, cadmium, cobalt and arsenic compounds are well known carcinogens to humans and experimental animals. In addition to the induction of mainly oxidative DNA damage, they interfere with nucleotide and base excision repair (BER) at low, non-cytotoxic concentrations. In case of arsenic, an inactivation of DNA repair has also been observed for the trivalent and pentavalent methylated metabolites, with the strongest effects exerted by MMA(III) and DMA(III). As potential molecular targets, interactions with so-called zinc finger proteins involved in DNA repair and/or DNA damage signaling have been identified. For example, arsenite suppresses poly(ADP-ribosyl)ation at extremely low, environmentally relevant concentrations. Also, Fpg and XPA involved in BER and NER, respectively, are inactivated by arsenite, MMA(III) and DMA(III). Nevertheless, an interaction with the zinc finger structures of DNA repair proteins may also occur by essential trace elements such as certain selenium compounds, which appear to exert anticarcinogenic properties at low concentrations but may compromise genetic stability at higher concentrations.