Glutathione Depletion Linked to Parkinson's Disease
Noel Peterson, N.D.
Corporate downsizing may be welcome on Wall Street, but when the brain's natural source for fighting free radical damage is drastically cut back, accumulating toxins may gain strength and accelerate the destruction of critical brain neurons.
According to many new studies, suboptimal levels of an important antioxidant called glutathione may underlie the progression of Parkinson's disease and ?other neurodegenerative disorders. Glutathione, it seems, protects cells from oxidative damage by mopping up excess free radicals.
Researchers found that when they reduced glutathione levels in rodent brain cells in vitro, two powerful toxins, peroxynitrite and sulfite, became much more damaging. Sulfite is found in pollution and food preservatives, and may accumulate to excess amounts as a result of disordered sulphur metabolism.
These two toxins have the ability to damage protein, DNA, lipids, and other parts of cells. By increasing their synergistic toxicity, deficiencies of glutathione may accelerate the neural damage associated with Parkinson's disease and other conditions, say researchers.
"The most striking aspect of our data is that a 50% depletion in GSH rendered cells very susceptible to the combined toxicities of sulfite and peroxynitrite." The drop in GSH made cells so vulnerable to destruction by these toxins, in fact, that the cells' ability to survive was "drastically reduced" to only 10%.
Interestingly, researchers have observed a similar depletion of glutathione in the substantia nigra, the dopamine-producing region of the brain, in patients with Parkinson's disease. This region of the brain often degenerates as the disease progresses.
Selenium deficiency leads to loss of glutathione. Glutathione levels can be effectively restored in patients with the supplement known as Recancostat.
Source: Marshall K-A, Reist M, Jenner P, Halliwell B. The neuronal toxicity of sulfite plus peroxynitrite is enhanced by glutathione depletion: implications for Parkinson's disease. Free Radic Biol and Med 1999;27(5):515-520.