Atoms often complete their outer shells by sharing electrons with other atoms. By sharing electrons, the atoms are bound together and satisfy the conditions of maximum stability for the molecule.⁵

Atoms and Molecules | Oxidation | Free Radicals | Chain Reaction | Multiple Effects | Antioxidants

Oxidation and reduction are redox chemical reactions. Most people can understand oxidation damage, as they are familiar with the process of rust formation of iron exposed to oxygen. Probably the most familiar free-radical reaction for most people is combustion (“burning”).⁶ In order for combustion to occur, the bond between the two oxygen atoms must be broken. This bond can be overcome by heat, requiring high temperatures, or the heat requirement can be lowered by enzymes to initiate reactions at the temperatures inside living things. Breaking such bonds and reforming of others will also create heat (energy).

Ironically, this energy-generation mechanism, which is so essential to life, can also set the stage for cell damage. The oxidation of foodstuffs (the conversion of food to energy) is like a controlled fire that liberates energy but can also let sparks fly, giving rise to potential damage. The sparks in this analogy are free electrons escaping the body’s “transport” system. These unpaired electrons readily form free radical molecules, which are chemically reactive and highly unstable.⁷

The two most important oxygen-centered free radicals are superoxide and hydroxyl radical. They are derived from molecular oxygen under reducing conditions. However, because of their reactivity, these same free radicals can participate in unwanted side reactions resulting in cell damage. Radicals requiring more energy to form are less stable than those requiring less energy.⁸

Atoms and Molecules | Oxidation | Free Radicals | Chain Reaction | Multiple Effects | Antioxidants

Normally, the bonds between atoms do not split in a way that leaves a molecule with an odd, unpaired electron. But when weak bonds split, free radicals are formed. Free radicals are very unstable and react quickly with other compounds, trying to capture the needed electron to gain stability. Generally, free radicals attack the nearest stable molecule, "stealing" its electron. When the "attacked" molecule loses its electron, it becomes a free radical itself, beginning a chain reaction. Once the process is started, it can cascade, finally resulting in the disruption of living cells.⁹

According to Gerhard Herzberg, who won the Nobel prize for his research of electronic structure and geometry of radicals, the preferred definition of free radicals is: "any transient (chemically unstable) species (atom, molecule, or ion)".¹⁰

The vast majority of free radicals that exist in your body at any given moment can be traced back to one of the following sources:

When free radicals steal an electron from a surrounding compound or molecule a new free radical is formed in its place. The newly formed radical then looks to return to its ground state by stealing electrons from cellular structures or molecules. Thus the chain reaction continues and can be "thousand of events long."¹⁴

The next two paragraphs are a little complex, included especially for those who want to know more technical details as they relate to the impact of free radicals on health. If you do not need such detail, skip to Multiple Effects.

Polyunsaturated fatty acids (PUFAs) are abundant in cellular membranes and in low-density lipoproteins (LDL).¹⁵ The PUFAs allow for fluidity of cellular membranes. A free radical prefers to steal electrons from the lipid membrane of a cell, initiating a free radical attack on the cell known as lipid peroxidation. Reactive oxygen species target the carbon-carbon double bond of polyunsaturated fatty acids. The double bond on the carbon weakens the carbon-hydrogen bond allowing for easy dissociation of the hydrogen by a free radical.¹⁶

A free radical will steal the single electron from the hydrogen associated with the carbon at the double bond. In turn this leaves the carbon with an unpaired electron and hence it becomes a free radical. In an effort to stabilize the carbon-centered free radical molecular rearrangement occurs. The newly arranged molecule is called a conjugated diene (CD). The CD then very easily reacts with oxygen to form a peroxy radical. The peroxy radical steals an electron from another lipid molecule in a process called propagation. This process then continues in a chain reaction.¹⁷

Atoms and Molecules | Oxidation | Free Radicals | Chain Reaction | Multiple Effects | Antioxidants

Damage caused by free radicals is currently believed to contribute to more than 70 disorders. These include:

Cell membranes are made of unsaturated lipids. The unsaturated lipid molecules of cell membranes are particularly susceptible to the damaging free radicals process and readily contribute to the uncontrolled chain reaction. Oxidative damage, another name for the chemical reaction that free radicals cause, can lead to a breakdown or even hardening of lipids, which make up all cell walls.

If the cell wall is hardened (lipid peroxidation) then it becomes impossible for the cell to properly get its nutrients, or to get signals from other cells to perform an action. Many other cellular activities can also be affected. In addition to the cell walls, other biological molecules are also susceptible to damage, including RNA, DNA and protein enzymes.

The primary site of free radical damage is the DNA found in the mitochondria. Mitochondria are small membrane-enclosed regions of a cell that produce the chemicals a cell uses for energy. Mitochondria are the "energy factories" of the cell.

Every cell contains an enormous set of molecules called DNA, which provide chemical instructions for a cell to function. This DNA is found in the nucleus of the cell, which serves as the "command center" of the cell, as well as in the mitochondria. The cell automatically fixes much of the damage done to nuclear DNA. However, the DNA in the mitochondria cannot be readily fixed.

Hence, this free radical generation process can disrupt all levels of cell function. This is why free radical damage is thought to underly so many conditions, including being such a basic mechanism of tissue injury. It damages us at the cellular level.¹⁸

Besides tissue injury, free radical damage is held to be responsible for premature aging. The free-radical theory of aging¹⁹ suggests that organisms age prematurely because cells accumulate free radical damage with the passage of time.

More recently, the relationship between disease and free radicals has led to the formulation of a greater generalization about the relationship between aging and free radicals. In its strong form, the hypothesis states that aging per se is a free radical process. The "weak" hypothesis holds that the degenerative diseases associated with aging generally involve free radical processes and that, cumulatively, these make you age. The latter is generally accepted, but the "strong" hypothesis awaits further proof. Both models trace back to Denham Harman's work.²⁰ Some of the scientific evidence includes:

Free radicals have also been implicated as playing a role in the etiology of cardiovascular disease and cancer.²⁶ Many forms of cancer are thought to be the result of reactions between free radicals and DNA, resulting in mutations that can adversely affect the cell cycle and potentially lead to malignancy.

Some of the symptoms of aging such as arteriosclerosis are also attributed to free-radical induced oxidation of many of the chemicals making up the body. In addition free radicals contribute to alcohol-induced liver damage, perhaps more than alcohol itself. Radicals in cigarette smoke have been implicated in inactivation of alpha 1-antitrypsin in the lung. This process promotes the development of emphysema.

Free radicals may also be involved in Parkinson's disease, senile and drug-induced deafness, schizophrenia, and Alzheimer's. The classic free-radical syndrome, the iron-storage disease hemochromatosis, is typically associated with a constellation of free-radical-related symptoms including movement disorder, psychosis, skin pigmentary melanin abnormalities, arthritis, and diabetes mellitus.²⁷

This free radical damage cannot be prevented or cured by any drugs - in fact most drugs are sources of MORE free radicals in the body.

Atoms and Molecules | Oxidation | Free Radicals | Chain Reaction | Multiple Effects | Antioxidants

Antioxidant means "against oxidation." Antioxidants work to protect other atoms from the effects of free radical attack, including protecting lipids from peroxidation. Antioxidants are effective because they are willing to give up their own electrons to free radicals. When a free radical gains the electron from an antioxidant it no longer needs to attack the cell and the chain reaction of oxidation is broken.²⁸

After donating an electron an antioxidant becomes a free radical by definition. However, antioxidants in this state are not harmful because they have the ability to accommodate the change in electrons without becoming reactive.²⁹

Because free radicals are necessary for life, the body has a number of mechanisms to minimize free radical induced damage and to repair the damage that does occur. These include the enzymes superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase.

In addition, antioxidants play a key role in these defence mechanisms. Some antioxidants are manufactured within the body and others can also be extracted from the food humans eat such as fruits, vegetables, seeds, nuts, meats, and oil. There are two lines of antioxidant defence within each cell.

The first line, found in the fat-soluble cellular membrane consists of vitamin E, beta-carotene, and coenzyme Q.³⁰ Of these, vitamin E is considered the most potent chain breaking antioxidant within the membrane of the cell. It is the primary defender against oxidation and lipid peroxidation

Inside the cell the second line, water soluble antioxidant scavengers, are present. These include vitamin C, glutathione peroxidase, superoxide dismutase (SD), and catalase.³¹ Vitamin C is the most abundant water-soluble antioxidant in the body. It acts primarily in cellular fluid. It is of particular note in combating free-radical formation caused by pollution and cigarette smoke. Also helps return vitamin E to its active form.³²

Further, there is good evidence bilirubin and uric acid can act as antioxidants to help neutralize certain free radicals. Bilirubin comes from the breakdown of red blood cells' contents, while uric acid is a breakdown product of purines. Too much bilirubin, though, can lead to jaundice, which could eventually damage the central nervous system, while too much uric acid causes gout.³³

So antioxidants neutralize free radicals by donating one of their own electrons, ending the electron-"stealing" reaction. The antioxidant nutrients themselves do not become free radicals after donating an electron because they are stable in either form (‘giving’ away the required number of electrons to become stable). They act as scavengers, helping to prevent cell and tissue damage that could lead to disease.

Although there are several enzyme systems within the body that scavenge free radicals, the principle micronutrient (vitamin) antioxidants are vitamin E, beta-carotene, and vitamin C. Additionally, selenium, a trace metal that is required for proper function of one of the body's antioxidant enzyme systems, is sometimes included in this category. The body cannot manufacture these micronutrients so they must be supplied in the diet.³⁴

Vitamin E : d-alpha tocopherol is a fat-soluble vitamin present in nuts, seeds, vegetable and fish oils, whole grains (esp. wheat germ), fortified cereals, and apricots. Current recommended daily allowance (USRDA³⁵) is 15 IU per day for men and 12 IU per day for women.³⁶

Vitamin C : Ascorbic acid is a water soluble vitamin present in citrus fruits and juices, green peppers, cabbage, spinach, broccoli, kale, cantaloupe, kiwifruit, and strawberries. The RDA is 60 mg per day. Intake above 2000 mg may be associated with adverse side effects in some individuals.³⁷

Beta-carotene is a precursor to vitamin A (retinol) and is present in liver, egg yolk, milk, butter, spinach, carrots, squash, broccoli, yams, tomato, cantaloupe, peaches, and grains. Because beta-carotene is converted to vitamin A by the body there is no set requirement. Instead the RDA is expressed as retinol equivalents (RE), to clarify the relationship. (NOTE: Vitamin A has no antioxidant properties and can be quite toxic when taken in excess.)³⁸

Here are some practical notes on how to prevent free radicals from significantly compromising your health³⁹: