In a previous post, we discussed the concept of oxidative stress and the association that it can have with numerous health concerns. It is also important to understand how the body controls free radicals and prevents oxidative stress from occurring. To review – we know that oxidative stress is the burden on the body as a result of an overproduction of free radicals. This occurs when the control mechanisms of the body that counter free radicals aren’t able to maintain a proper balance. The cause of this imbalance is often attributed to a stressor such as an immune reaction or environmental exposure. It is important to note that free radicals do not always have negative effects on the body; a problem only arises when the amount of free radicals is high enough to outweigh the body’s normal antioxidant defenses.
The body has several ways to deal with an excess of free radicals. The first line of defense includes the antioxidant enzymes superoxide dismutase (SOD), glutathione peroxidase, and catalase. These enzymes help rid the body of free radicals by converting them into water and oxygen (Figure 1). After oxygen becomes a free radical, SOD converts it into hydrogen peroxide, then catalase and glutathione peroxidase continue the conversion into water and oxygen.
The enzymes discussed above are the first line of defense against free radicals. Their optimal function is dependent on certain antioxidants and mineral cofactors derived from the diet. Polyphenols, vitamins E and C, coenzyme Q10, and glutathione support the antioxidant enzymes. The body makes every effort to minimize the negative effects of free radicals by relying on its own enzymes, as well as antioxidants from the diet. Deficiencies in either of these defense systems can lead to a wide variety of oxidative stress-related clinical symptoms and conditions.
Guest author: Deanna Fall is currently a scientific writer and research analyst for NeuroScience, Inc. and holds a bachelor’s degree in biology from Ferris State University in Big Rapids, Michigan and a master’s degree in health informatics at the University of Minnesota. Deanna joined NeuroScience in 2009 with experience in pharmaceutical research and development in the field of neurotoxicology.