Individuals suffering from ADHD are under high levels of oxidative stress in their brain. Our main protective shield is the master antioxidant glutathione. Poor blood sugar control and high environmental toxin exposure are known to deplete glutathione levels and impair mitochondrial function.
A key pathway that maintains cellular glutathione levels and the ability of the cell to adapt to stress is called Keap1-Nrf2. When this pathway breaks down it causes increased levels of oxidative stress within the cell that leads to the glutathione depletion and mitochondrial dysfunction. Improving glutathione status in ADHD individuals improves hyperactivity and focus.
Glutathione depletion and oxidative stress.
Oxidative stress is believed to contribute to the pathogenesis of Parkinson’s disease. One of the indices of oxidative stress is the depletion of the antioxidant glutathione (GSH), which may occur early in the development of Parkinson’s disease. To study the role of GSH depletion in the survival of dopamine neurons we treated mesencephalic cultures with the GSH synthesis inhibitor L-buthionine sulfoximine.
Our studies have shown that the depletion of GSH causes a cascade of events, which ultimately may result in cell death. An early event following GSH depletion is a phospholipase A(2)-dependent release of arachidonic acid. Arachidonic acid can cause damage to the GSH-depleted cells through its metabolism by lipoxygenase. The generation of superoxide radicals during the metabolism of arachidonic acid is likely to play an important role in the toxic events that follow GSH depletion.