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Free radicals and antioxidants in health and disease

Free radicals are oxygen-containing chemicals that have an impaired electron. The impaired electron makes free radicals highly reactive to DNA, proteins, membranes, and other cell machineries, resulting in oxidative damages including DNA mutations, protein dysfunction, and destruction of membrane and other cell structures. These oxidative damages promote aging and increase the risk of age-related diseases such as cancer, cardiovascular diseases, immune system declines, brain dysfunction, and cataracts. Known free radicals that are involved in the aging process are superoxide, hydrogen peroxide (H2O2), hydroxyl radical (OH), singlet oxygen, lipid epoxides, lipid hydroperoxides, lipid alkoyl, peroxyl radicals, and oxides. They are either produced during our normal metabolisms or introduced into our bodies from outside sources.[1]

Some externally generated sources of free radicals are :

  • cigarette smoke
  • environmental pollutants
  • radiation
  • ultraviolet light
  • certain drugs, pesticides, anaesthetics and industrial solvents
  • ozone

The free radical diseases

A well accepted fact is the increasing incidence of disease with advancing age.  A plausible explanation for the association of age and disease is based on the implication of free radical reactions in the pathogenesis of several disorders.

Free radical reactions are expected to produce progressive adverse changes that accumulate with age throughout the body.  Such “normal” changes with age are relatively common to all. However, superimposed on this common pattern are patterns influenced by genetics and environmental differences that modulate free radical damage. These are manifested as diseases at certain ages determined by genetic and environmental factors. Cancer and atherosclerosis, two major causes of death, are salient “free radical” diseases. Cancer initiation and promotion is associated with chromosomal defects and oncogene activation. It is possible that endogenous free radical reactions, like those initiated by ionizing radiation, may result in tumour formation. The highly significant correlation between consumption of fats and oils and death rates from leukaemia and malignant neoplasia of the breast, ovaries and rectum among persons over 55 years may be a reflection of greater lipid peroxidation [2]. Studies on atherosclerosis reveal the probability that the disease may be due to free radical reactions involving diet-derived lipids in the arterial wall and serum to yield peroxides and other substances. These compounds induce endothelial cell injury and produce changes in the arterial walls [3].

Free radicals, however, are not always harmful. They also serve useful purposes in the human body. Several observations indicate that the oxygen radicals in living systems are probably necessary compounds in the maturation processes of cellular structures. Furthermore, white blood cells release free radicals to destroy invading pathogenic microbes as part of the body’s defence mechanism against disease. Hence, the complete elimination of these radicals would not only be impossible, but also harmful.

References

  1. Langseth L. Oxidants, antioxidants and disease prevention. Belgium, International Life Science Institute, 1996.
  2. Lea AJ. Dietary factors associated with death rates from certain neoplasms in man. Lancet, 1966, 2:332-3.
  3. Harman D. Role of free radicals in aging and disease. Annals of New York Academy of Sciences, 1992, 673:126-141.