What We Do

Scientists in our program study free radicals, the highly reactive molecules capable of inducing oxidative damage to DNA, protein, and lipids. The intra- and extracellular content of these species increase during a variety of diseases. Free radical damage is therefore believed to contribute to the accompanying degeneration of physiologic function. Paradoxically, free radicals are also generated in response to normal physiologic stimuli and can exert reversible effects on protein function indicative of metabolic regulation.
The research being conducted by scientists within the Free Radical Biology and Aging Program focuses on establishing mechanisms by which free radicals regulate physiologic function and, conversely, exert deleterious effects during the progression of specific pathophysiologic events. Chemical, biochemical, and physiological approaches are employed to define pathways of free radical production and removal, structural and functional alterations to biomolecules induced by free radicals, and novel aspects of mitochondrial bioenergetics and sulfur metabolism that impact these processes.
Disease related areas of investigation focus on the role of free radicals in various pulmonary (asthma), musculoskeletal (osteoarthritis), and cardiovascular (ischemia/reperfusion and heart failure) disorders associated with the aging process and exacerbated by obesity and systemic inflammation.
Our Publications

2011
Baily CN, Cason RW, Vadvalkar SS, Matsuzaki S, Humphries KM. Inhibition of mitochondrial respiration by phosphoenolpyruvate. Arch Biochem Biophys 514:68-74, 2011. [Abstract]
Dasuri K, Zhang L, Ebenezer P, Fernandez-Kim SO, Bruce-Keller AJ, Szweda LI, Keller JN. Proteasome alterations during adipose differentiation and aging: links to impaired adipocyte differentiation and development of oxidative stress. Free Radic Biol Med 51:1727-1735, 2011. [Abstract]
Matsuzaki S, Kotake Y, Humphries KM. Identification of mitochondrial electron transport chain-mediated NADH radical formation by EPR spin-trapping techniques. Biochemistry 50:10792-10803, 2011. [Abstract]
McLain AL, Szweda PA, Szweda LI. alpha-Ketoglutarate dehydrogenase: A mitochondrial redox sensor. Free Radic Res 45:29-36, 2011. [Abstract]
Talbot JJ, Shillingford JM, Vasanth S, Doerr N, Mukherjee S, Kinter MT, Watnick T, Weimbs T. Polycystin-1 regulates STAT activity by a dual mechanism. Proc Natl Acad Sci U S A 108:7985-7990, 2011. [Abstract]
2012
Griffin TM, Huebner JL, Kraus VB, Yan Z, Guilak F. Induction of osteoarthritis and metabolic inflammation by a very high fat diet in mice: Effects of short-term exercise. Arthritis Rheum 64:443-453, 2012. [Abstract]
Zhu X, Castellani RJ, Moreira PI, Aliev G, Shenk JC, Siedlak SL, Harris PL, Fujioka H, Sayre LM, Szweda PA, Szweda LI, Smith MA, Perry G. Hydroxynonenal-generated crosslinking fluorophore accumulation in Alzheimer disease reveals a dichotomy of protein turnover. Free Radic Biol Med 52:699-704, 2012. [Abstract]
* Indicates publications by more than one department.
Contact Us

Free Radical Biology & Aging Research Program
Oklahoma Medical Research Foundation
825 NE 13th Street, MS 21
Oklahoma City, OK 73104
Phone: (405) 271-7570
Fax: (405) 271-1437
Email: evansj@omrf.org




