Research by neuroscientists at the University of Virginia Health System shows that oxygen free radicals are damaging proteins in mitochondria, the tiny cellular 'batteries' of brain cells.
This damage may be one main cause of Parkinson's Disease (PD), the chronic movement disorder that affects at least one million Americans. UVa scientists believe the damage is taking place in a large protein structure called complex I, the first stop in the electron transport chain, which produces an electrical charge inside mitochondria. Mitochondria then use this electrical charge to make energy.
Using the brain cells from deceased Parkinson's patients who donated to the UVa brain bank, Dr. Jim Bennett, a UVa neurologist, and colleagues, isolated complex I from the mitochondria of ten Parkinson's brains and compared them to the complex I proteins from twelve normal brains. They discovered that the complex I assembly in Parkinson's had 50 percent more damage from oxygen. The complex I in Parkinson's brains also had evidence of not being properly assembled and had reduced electron flow, Bennett said.
"This part of the protein complex is being damaged by oxygen free radicals more in a brain with Parkinson's than it is in someone of same age who does not have PD," Bennett said. His research is published in the Journal of Neuroscience.
Oxygen free radicals are oxygen molecules that carry an extra electron. They are destructive because, in excessive amounts, they chemically attack the components of the cell, including proteins, DNA and lipids in cell membranes. One of the major problems of normal aging is an increased level of these free radical damaged proteins, along with damaged DNA and lipids.