Free Radical Biology & Aging Research Program
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 Scientists
Our Publications

2013
Bhatnagar A, Unal H, Jagannathan R, Kaveti S, Duan ZH, Yong S, Vasanji A, Kinter M, Desnoyer R, Karnik SS. Interaction of G-Protein betagamma Complex with Chromatin Modulates GPCR-Dependent Gene Regulation. PLoS One 8:e52689, 2013. [Abstract]
Ghosh S, Willard B, Comhair S, Dibello P, Xu W, Shiva S, Aulak KS, Kinter M, Erzurum SC. Disulfide bond as a switch for copper-zinc superoxide dismutase activity in asthma. Antioxid Redox Signal 18:412-423, 2013. [Abstract]
Hallgren KW, Zhang D, Kinter M, Willard B, Berkner KL. Methylation of gamma-carboxylated Glu (Gla) allows detection by liquid chromatography-mass spectrometry and the identification of Gla residues in the gamma-glutamyl carboxylase. J Proteome Res 2013. [Abstract] EPub
Macdonald MJ, Langberg EC, Tibell A, Sabat G, Kendrick MA, Szweda LI, Ostenson CG. Identification of ATP Synthase As a Lipid Peroxide Protein Adduct in Pancreatic Islets From Humans With and Without Type 2 Diabetes Mellitus. J Clin Endocrinol Metab 98:E727-E731, 2013. [Abstract]
McLain AL, Cormier PJ, Kinter M, Szweda LI. Glutathionylation of alpha-Ketoglutarate Dehydrogenase: The Chemical Nature and Relative Susceptibility of the Cofactor Lipoic Acid to Modification. Free Radic Biol Med 2013. [Abstract] EPub
O'Conor CJ, Griffin TM, Liedtke W, Guilak F. Increased susceptibility of Trpv4-deficient mice to obesity and obesity-induced osteoarthritis with very high-fat diet. Ann Rheum Dis 72:300-304, 2013. [Abstract]
Perry EA, Castellani RJ, Moreira PI, Nunomura AA, Liu Q, Harris PL, Sayre LM, Szweda PA, Szweda LI, Zhu X, Smith MA, Perry G. Neurofilaments are the Major Neuronal Target of Hydroxynonenal Mediated Protein Crosslinks. Free Radic Res 2013. [Abstract] EPub
Rindler PM, Plafker SM, Szweda LI, Kinter M. High dietary fat selectively increases catalase expression within cardiac mitochondria. J Biol Chem 288:1979-1990,2013. [Abstract]
Vadvalkar SS, Baily CN, Matsuzaki S, West M, Tesiram YA, Humphries KM. Metabolic inflexibility and protein lysine acetylation in heart mitochondria of a chronic model of Type 1 diabetes. Biochem J 449:253-261, 2013. [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: Jeannie-Evans@omrf.org

Scott M. Plafker, Ph.D., R.Ph.

