Professor of Chemistry
College of Engineering, Computing and Applied Sciences
Contact: 864-656-0481 or firstname.lastname@example.org
Dr. Brumaghim earned her Ph.D. in organometallic chemistry from the University of Illinois at Urbana-Champaign. She then completed an NIH post-doctoral fellowship with Dr. Ken Raymond in the Department of Chemistry at the University of California at Berkeley, followed by a second post-doctoral appointment with Dr. Stuart Linn in the Department of Molecular and Cellular Biology, also at Berkeley. Her strong background in inorganic and bioinorganic chemistry has led her research at Clemson to focus on the ability of several antioxidant classes to prevent metal-mediated oxidative damage. This oxidative damage is responsible for cell death during oxidative stress and leads to a wide variety of pathologies, including cardiovascular disease, cancer, and neurodegenerative diseases. However, due to the lack of readily deployable tools to study such damage and a lack of understanding about cellular metal-based processes, metal-mediated oxidative DNA damage is often overlooked for other, easier-to-study pathways. Dr. Brumaghim has developed tools to quantify antioxidant prevention of metal-mediated oxidative damage, and has demonstrated the first quantitatively predictive, structure-activity relationships for a variety of different antioxidant classes.
For more information, see her Curriculum Vitae.
The potential of antioxidants for treating, and more importantly preventing, disease is widely recognized, but antioxidants have not proven decisively useful in clinical trials. One reason for this is that tens of thousands of antioxidants are known, and testing even a significant fraction of those in clinical trials is practically impossible. Dr. Brumaghim is the first to identify a new mechanism for the activity of several antioxidant classes (prevention of metal-mediated DNA damage) and to establish predictive models for their behavior. These models have been validated in biochemical assays and bacterial cells, and initial results seem to demonstrate the validity of these models in human cell cultures as well. It is her sincere hope that rationally selected antioxidants will be used in future, mechanistically-sound clinical trials that could transform the prevention of diseases caused by oxidative stress such as cancer, cardiovascular disease, and neurodegenerative diseases.
Antioxidants, Metals, Oxidative damage, DNA damage, Iron, Copper, Selenium, Sulfur, Polyphenols