CHED 1145 |
| The detrimental effects of NO production in vivo can occur as a result of oxidation of NO, which occurs spontaneously in aerobic environments. This autoxidation reaction can form harmful higher nitrogen oxides, which are capable of oxidizing and nitrosating proteins, lipids, and DNA, potentially leading to tissue injury, disease, and cancer. It is well known that autoxidation of NO in the gas phase produces such intermediates, particularly nitrogen dioxide (NO2) and dinitrogen trioxide (N2O3). The mechanism of NO autoxidation in aqueous media has commonly been assumed to be analogous to the gas phase reaction, with the extension of N2O3 hydrolysis to form nitrite (NO2-). We propose that NO autoxidation within cells occurs through a mechanism that is fundamentally different from the gas phase reaction, producing variants of the above intermediates that possess distinct nitrosative and oxidative capabilities. Although the rate constant for aqueous NO autoxidation has been determined to be similar to the gas phase reaction, preliminary results support a unique mechanism. The characterization of aqueous phase NO autoxidation is thus critical to fully understanding of NO in biological systems, particularly in terms of pathophysiology. Gas phase NO autoxidation can be effectively mimicked in water by reaction of NO with 2-phenyl-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (PTIO), which yields free NO2 via oxygen transfer. Using trapping agents of oxidation, nitrosation, and nitration in conjunction with PTIO, we will elucidate the intermediates of NO autoxidation by colorimetric and flourometric assays. Using such competitive kinetics techniques, new insight into the mechanism of NO autoxidation can be achieved. |
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Undergraduate Research Poster Session: Inorganic Chemistry
2:00 PM-4:00 PM, Monday, April 7, 2008 Morial Convention Center -- Hall A, Poster
Division of Chemical Education |