The Impact of Oxidative and Carbonyl Stress on Cell Function: Functional Consequences for Macrophages

Abstract

There is a growing body of evidence demonstrating that products of oxidative stress, namely carbonyl adducts, play a major role in chronic inflammation as well as age-related diseases. Their involvement crosses a broad spectrum of medical conditions encompassing airway diseases, such as asthma and COPD (chronic obstructive pulmonary disease) [1], neurodegenerative disorders like alzheimers [2], the cardiovascular disease atherosclerosis [3], and the arthritic diseases rheumatoid arthritis [4] and osteoarthritis [5]. Several good reviews exist highlighting the importance of carbonyl adducts in disease [6-8]. Not only do carbonyl adducts act as simple markers of tissue damage by oxidative stress, but they are able to participate in disease pathogenesis. This is accomplished through post-translational modification of protein, be it intra- or extra-cellular, the net effect being to alter cell function with the eventual tissue damage that follows [9-12].

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