Saturday, October 13, 2012: 3:20 AM
Hall 4E/F (WSCC)
There are numerous health effects that arise from exposure to metals. Arsenic and uranium naturally occur in the environment and individuals are commonly exposed to these metals by inhalation and ingestion. Many Navajo people have been, and continue to be, exposed to uranium through the legacy of uranium mining. 1100 abandoned Cold War uranium waste sites remain within Navajo communities and numerous wells exceed maximum contaminant levels for uranium and other metals such as arsenic. It is known that certain metals can disrupt protein function by interacting with zinc finger structures and thus inhibit important cellular processes including DNA repair. Based on this mechanism, many metals are now viewed as co-carcinogens and amplify the DNA damaging capacity and tumorigenicity of other carcinogens. The carcinogenicity of uranium is well established in the literature, but there is little known regarding uranium interaction with zinc finger protein structures. Our work with arsenic demonstrates that very low levels of arsenic causes zinc depletion from target zinc finger DNA repair proteins leading to increased DNA damage and mutagenesis that can be reversed by zinc. Based on these findings, we investigated the effect of uranium on DNA repair and the activity of a specific zinc finger DNA repair protein target (PARP-1). Preliminary findings suggest that one mechanism of uranium toxicity may rely on disruption of zinc finger protein function, raising the possibility that zinc supplementation could offset some aspects of uranium toxicity.