Free radical tissue damage: protective role of antioxidant nutrients ¹

Abstract

Highly reactive molecules called free radicals can cause tissue damage by reacting with polyunsaturated fatty acids in cellular membranes, nucleotides in DNA, and critical sulfhydryl bonds in proteins. Free radicals can originate endogenously from normal metabolic reactions or exogenously as components of tobacco smoke and air pollutants and indirectly through the metabolism of certain solvents, drugs, and pesticides as well as through exposure to radiation. There is some evidence that free radical damage contributes to the etiology of many chronic health problems such as emphysema, cardiovascular and inflammatory diseases, cataracts, and cancer. Defenses against free radical damage include tocopherol (vitamin E), ascorbic acid (vitamin C), beta-carotene, glutathione, uric acid, bilirubin, and several metalloenzymes including glutathione peroxidase (selenium), catalase (iron), and superoxide dismutase (copper, zinc, manganese) and proteins such as ceruloplasmin (copper). The extent of tissue damage is the result of the balance between the free radicals generated and the antioxidant protective defense system. Several dietary micronutrients contribute greatly to the protective system. Based on the growing interest in free radical biology and the lack of effective therapies for many of the chronic diseases, the usefulness of essential, safe nutrients in protecting against the adverse effects of oxidative injury warrants further study.

Effects of Chard (Beta vulgarisL. var cicla) on the Liver of the Diabetic Rats: A Morphological and Biochemical Study

“…39) Free radicals formed during the reduction of O 2 , such as peroxy-, hydroxy-, and superoxide radicals, are known to cause cell damage directly or indirectly. 40) Previous animal studies show that persistent hyperglycemia causes increased production of reactive oxygen species through glucose autooxidation and NEG, which in turn causes increased oxidative stress. 41) GSH, the most important biomolecule against chemically induced toxicity, can participate in the elimination of reactive intermediates by reduction of hydroperoxides in the presence of GP x .…”

Effects of Intraperitoneally Administered Lipoic Acid, Vitamin E, and Linalool on the Level of Total Lipid and Fatty Acids in Guinea Pig Brain with Oxidative Stress Induced by H2O2

“…Endogenous sources of ROS in aerobic mammalian cells are the mitochondrial electron carriers and enzymes. Representative external sources include redox cycling drugs, radiation, and various lifestyle and environmental influences, such as smoking, drinking alcohol, excessive exercise, pollution, and overexposure to the sun (Machlin and Bendich, 1987;Dizdaroglu, 1993). The highlyreactive superoxide radical and hydrogen peroxide may be toxic to cells by a direct attack at the molecular level, or indirectly by generating secondary reactive species such as the hydroxyl radical (Brenneisen et al, 1997).…”

Association Between Toenail Selenium and Risk of Acute Myocardial Infarction in European Men: The EURAMIC Study

“…However, in other studies, this association could not be confirmed (7)(8)(9)(10). Antioxidant defense is achieved by additive or synergistic action of enzymes and antiox-idant nutrients (11,12). Selenium and vitamin E in particular appear to have overlapping and partly compensative functions (13)(14)(15)(16)(17).…”