How the very thing that keeps us alive is also trying to kill us.
Human beings, as well as many of Earth’s creatures, are aerobic in nature. To maintain active muscles, our cells require a copious amount of oxygen; the same principle applies to our most vital organ, the brain, down to our most intricate of capillaries. Oxygen is an essential element in energy metabolization, gas exchange, and almost every other bodily process. Aside from anaerobic species, life truly would not persist without oxygen. Yet, an extreme irony exists in the constant biological processes of our bodies. Oxygen undergoes changes as it is utilized in our sundry biological pathways, and these changes tend to transform what is regularly a vital molecule into dangerously poisonous agents known as “Reactive Oxygen Species”.
One of the most common of these Species is superoxide, a malformed version of oxygen produced during an oxygen molecule’s passage through a cell’s mitochondria. Mitochondria are found within each of our cells, and are responsible for transforming food into usable cellular energy. As oxygen proceeds through these mitochondrial pathways, it becomes partially reduced; molecules become reduced by acquiring an extra electron. In this case, oxygen has gained an electron, transforming it into the molecule superoxide. This extra, unpaired electron changes the behavior of the molecule as it searches for another electron to bind to. Superoxide, with its unpaired electron, is therefore a radical element and will more readily bind to other radical elements.
This production of superoxide is natural in a normally operating aerobic metabolism. While most superoxide is produced internally (white blood cell activity also yields large amounts of superoxide), external sources such as cigarette smoke and exposure to ultraviolet light also cause increased levels of superoxide. As superoxide becomes present in our bodies, it is often converted into other “Reactive Oxygen Species”. ROS are known to cause damage to many biological molecules. Hydroxyl radicals, formed when superoxide is in the presence of iron or copper, can damage cell membranes and lipoproteins, particles that store cholesterol and fat. Proteins may be damaged by other ROS, causing structural changes and loss of enzyme activity. Another threat is made to our DNA which is estimated to sustain 10,000 “oxidative hits” per day. Although DNA repair enzymes can reverse much of the damage, their success rate is not perfect. Lesions accrued by ROS cause mutations that accumulate with age and may contribute to cancer. ROS damage is also implicated in heart disease and degenerative diseases, such as atherosclerosis.
Fortunately, nature has provided a way to prevent damage caused by these Reactive Oxygen Species. Antioxidants from our diet collect ROS before they cause damage. Inside our cells, antioxidant enzymes scavenge for harmful radicals and convert them into less threatening species. The existence of these evolved enzymes is considerable proof towards the threat of oxidative damage to cellular survival. Additional proof comes from a recent discovery that noted a defective antioxidant enzyme (superoxide dismutase) in individuals with Lou Gehrig’s disease.
In blood and extracellular fluid, small, molecular antioxidants take up the job of their enzymatic counterparts. Molecular antioxidants may be lipid or water soluble, depending on where they operate in the body. Vitamin E is the most abundant of the lipid soluble antioxidants. Found mainly in nuts and seeds, vitamin E is vital protection against oxidation and has been found in studies to substantially reduce the risk of heart disease. Vitamins A and C also serve as antioxidants within the body, and may help prevent cancer, heart disease, and degenerative diseases. Because humans do not synthesize antioxidants naturally, it is important to maintain a diet that will supply them. These dietary antioxidants, found primarily in fruits, vegetables, nuts, and seeds, are the best protection against ROS; they are vital to protect the body’s biological molecules and to prevent age-related degenerative diseases.
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