Oxygen Radicals & Autism
Overloaded?: Oxygen Radicals & Autism
Oxygen radicals damage the brain and nervous system
Autistic children's inability to combat oxidative stress can lead to many health problems. Oxidative stress is caused by oxygen radicals — highly unstable chemicals that react with and destroy healthy cells. These free oxygen radicals are produced by the body in manageable amounts as byproducts of normal body metabolism, but their prevalence can be exacerbated by exposure to environmental chemicals. Oxygen radicals damage cells by reacting with proteins, DNA, carbohydrates, and fats, setting off chain reactions that can only be stopped by a cell's antioxidant defense system. In the process they disrupt cell functions and interfere with signals sent between cells in the body, which can lead to auto-immunity (Klein 2003).
Oxidative damage is counteracted by the body's antioxidant systems, which convert oxygen radicals into harmless byproducts. Oxidative stress occurs when oxygen radicals overwhelm the capacity of the body's antioxidant systems. Oxidative stress affects many body systems. It damages cell membrane structure (lipids), the cell machinery that performs the essential work of the cells (proteins), and the body's ability to regulate cell growth and protein synthesis (DNA and RNA). Oxidative stress is associated with premature aging of cells, and can lead to tissue inflammation, damaged cell membranes, autoimmunity and cell death (Klein 2003). Glutathione is the most important antioxidant for metals detoxification and excretion.
The brain and nervous system are particularly vulnerable to oxidative stress due to limited antioxidant capacity. The brain makes up about two percent of a person's mass but consumes 20 percent of their metabolic oxygen. The vast majority of this energy is used by the neurons (Shulman 2004). Some brain cells, like neurons, cannot make glutathione, but instead rely on surrounding astrocyte cells to provide useable glutathione precursors. Because the brain has limited access to the bulk of antioxidants produced by the body, neurons are the first cells to be affected by a shortage of antioxidants, and are most susceptible to oxidative stress. Researchers studying antioxidant protection of neurons are finding short windows during development of high vulnerability to oxidative stress (Perry 2004).
Children are more vulnerable than adults to oxidative stress due to their naturally low glutathione levels from conception through infancy (Erden-Inal 2003, Ono 2001). Risks created by this natural deficit in detoxification capacity in infants are compounded by the fact that mercury and other environmental chemicals that invoke oxidative stress are found at higher concentrations in the developing infant than in their mothers and appear to accumulate in the placenta.
In addition to this natural variability in antioxidant status with age, a person's genes play a strong role in their ability to make antioxidants in response to oxidative stress. A host of genes determine the speed and responsiveness of antioxidant production and recycling. Some genes common in one quarter to one half of the U.S. population reduce glutathione activity and are linked with increased odds of several cancers (Hallier 1994, Engel 2002). People with gene deletions for two types of glutathione genes (GST M1 and T1) are more likely to have allergic reactions to the mercury-based preservative thimerosal (Westphal 2000).