Mitochondrial oxidative damage and human diseases

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A number of human diseases are associated with increased cell death caused by free radicals. These include degenerative diseases such as Parkinson's disease, Friedreich's ataxia and diabetes. Free radicals are reactive by-products of normal metabolism that damage cell components thereby disrupting normal function and leading to cell death. Mitochondria are the major source of free radicals within cells. These free radicals are formed as mitochondria consume the oxygen we breathe to make energy available to the cell. Mitochondria are also central to determining how cells die, consequently free radical damage to mitochondria is an important cause of cell death. We have developed procedures to target novel molecules to mitochondria. The hope is that these new molecules will enable us to elucidate the mechanisms by which free radicals damage mitochondria and increase cell death in human diseases. Some of these molecules are antioxidants that should block the effects of free radicals. Therefore this approach may also lead to novel therapies to decrease mitochondrial oxidative stress in human diseases such as Alzheimer's Disease and Parkinson's Disease.