Oxidative Damage

The area of oxidative stress and lipid peroxidation has been a major research focus at Vanderbilt for the past three decades, and the P30 NIEHS Core Center has supported much of the work in this area. Lipid peroxidation results from a variety of environmental insults, and antioxidants play a critical role as defense mechanisms against this free radical chain process.  In addition to the peroxide and hydroperoxide primary products of the oxidation reaction, complex oxygenated secondary products are formed (i.e., 4-hydroxynonenal). Among these products are electrophiles that are commonly recognized to be cyto- and genotoxic. A new understanding of the mechanisms of peroxidation and the action of antioxidants has developed in recent years, and this P30 EHS Core Center and the collaborative research programs in the Oxidative Damage program (including an NIEHS-funded program project grant) offer the opportunity to probe these processes in vivo. Oxidant stress is implicated in multiple environmental and lifestyle-associated diseases, including neurodegenerative, cardiovascular, and pulmonary disorders. The research focus of investigators studying oxidative stress involves the role of lipid mediators in human disease. The following efforts are currently underway:

• The major products of lipid peroxidation associated with human cardiovascular disease and other disorders are being identified.
• Novel and potent antioxidants are being examined for their ability to prevent oxidant stress, and by implication, diseases associated with it.
• The beneficial effects of omega-3 fatty acids are being expanded in the prevention of cardiovascular and neurodegenerative disorders.
• Basic mechanisms involved in cellular processes associated with oxidant stress and human disease are being studied.
• Unique biomarkers that result from adduction of lipids to proteins (and are implicated in the pathophysiology of atherosclerosis) are being identified, offering a unique opportunity to define the role of lipid peroxidation and its inhibition in human disease.

For further detail on research programs focusing on Oxidative Damage, see the individual faculty pages of Brown, Burk, Guengerich, Hartert, Ikizler, Liebler, Marnett, and Porter.