Controlled Accentuation of Reactive Oxygen Species in Cancer Cell Models by Redox-Active Molecular Probes
Location
Room 2905 A
Session Format
Paper Presentation
Research Area Topic:
Natural & Physical Sciences - Chemistry
Abstract
Normal cellular metabolism generates intracellular by-products identified as reactive oxygen species (ROS). While ROS levels are safely maintained by the antioxidant pathway, the rapid metabolism of cancer cells causes unusually high levels of ROS. These cells survive due to the continued function of antioxidants, but the equilibrium between ROS generation and ROS reduction by antioxidants is significantly closer to lethal ROS levels than that of healthy cells. To capitalize on this difference, we have synthesized and continue to mechanistically study various gold N-heterocyclic carbenes that incorporate additional redox-active moieties capable of influencing ROS levels in cancer cells. These efforts have led to the development of complexes capable of inducing enhanced ROS formation and persistence by targeting antioxidant pathways via multiple mechanisms. Multiple human carcinoma cell lines have been utilized in this research to model the action of these complexes in different tumor types.
Presentation Type and Release Option
Presentation (Open Access)
Start Date
4-16-2016 4:00 PM
End Date
4-16-2016 5:00 PM
Recommended Citation
McCall, Rebecca Erin, "Controlled Accentuation of Reactive Oxygen Species in Cancer Cell Models by Redox-Active Molecular Probes" (2016). GS4 Georgia Southern Student Scholars Symposium. 116.
https://digitalcommons.georgiasouthern.edu/research_symposium/2016/2016/116
Controlled Accentuation of Reactive Oxygen Species in Cancer Cell Models by Redox-Active Molecular Probes
Room 2905 A
Normal cellular metabolism generates intracellular by-products identified as reactive oxygen species (ROS). While ROS levels are safely maintained by the antioxidant pathway, the rapid metabolism of cancer cells causes unusually high levels of ROS. These cells survive due to the continued function of antioxidants, but the equilibrium between ROS generation and ROS reduction by antioxidants is significantly closer to lethal ROS levels than that of healthy cells. To capitalize on this difference, we have synthesized and continue to mechanistically study various gold N-heterocyclic carbenes that incorporate additional redox-active moieties capable of influencing ROS levels in cancer cells. These efforts have led to the development of complexes capable of inducing enhanced ROS formation and persistence by targeting antioxidant pathways via multiple mechanisms. Multiple human carcinoma cell lines have been utilized in this research to model the action of these complexes in different tumor types.
