Biography

Dr. Tak Yee Aw was a graduate of the University of Otago, New Zealand (Ph.D. Biochemistry). She received postdoctoral training at the University of California, Los Angeles, and Emory University, Atlanta before joining the Physiology Department in 1990. Dr. Aw has served on grant review panels for numerous international funding agencies, the American Heart Association, and was a member of the Nutrition (1995-99) and Gastrointestinal Cell and Molecular Biology (GCMB, 2004-08) study sections of the National Institutes of Health. She has served as Co-Chair of the Sunrise Free Radical School, SFRBM (2005-07), and is currently on the Editorial Board of Free Radical Biology & Medicine, American Journal of Physiology (GI/Liver section), and Pathophysiology. Dr Aw has received continuous NIH funding since 1992, and has over 140 publications.

Research

Tissue oxidative stress underpins many malignant transformations and degenerative diseases. Reactive oxygen species (ROS) derived from mitochondrial respiration, cell metabolism, and exogenous sources disrupt cellular oxidation-reduction (redox) balance that governs metabolic fidelity and cell fate. My laboratory examines the role of glutathione/glutathione disulfide (GSH/GSSG), a major cellular thiol antioxidant redox system, in regulating cell death/survival and cytoprotective mechanisms. Ongoing research addresses two major areas:

Oxidative stress and mitochondrial integrity. Mitochondria, apart from ATP generation, are sentinel in cell survival and are vulnerable to oxidative damage. This research investigates the role of oxidative stress on mitochondrial protein and DNA damage, the function of GSH redox in repair, and how loss of mitochondrial integrity orchestrates apoptotic death. Research further addresses the link between mitochondrial GSH and pyridine nucleotide [NAD/NADH] redox and its implication for mitochondrial function and cellular reducing capacity.

Oxidative stress and degenerative disorders. Chronic and systemic oxidative stress induces tissue death and organ degeneration such as occurs in neurodegeneration and diabetes. This research investigates the role of GSH redox and growth factors (e.g., insulin) in controlling cell signaling, gene transcription and mechanisms in enzyme expression and the contribution of GSH redox homeostasis to neurovascular cell integrity and survival.

Figure Legend. Detection of ROS production in mitochondria in control (top) and oxidant-treated (bottom) neuronal (PC12) cells. Green fluorescence maps mitochondria location; red fluorescence denotes ROS presence; orange/yellow co-localizes ROS with mitochondria.

Laboratory techniques

Experimental models: cell culture (colonic, neuronal & neurovascular cell lines); chemical/genetically engineered models of diabetes and antioxidant deficiencies

Analytical methods: HPLC, dual wavelength spectrophotometry, fluorescence spectrometry, flow cytometry, assays of: GSH/GSSG, pyridine nucleotides, mitochondrial ROS and metabolites, DNA damage, cell apoptosis & proliferation.