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ANTIOXIDANTS > back to About Micronutrients A wide range of health conditions can develop or be worsened by the presence of highly reactive and unstable oxygen molecules referred to as reactive oxygen species, or free radicals, which cause oxidative stress. Free radicals are by-products that are formed in the body when fat molecules react with oxygen - the way a peeled apple turns brown or silver tarnishes when exposed to air. Some of the more common free radical molecules include hydroxyl radical, peroxides, singlet oxygen and superoxide, which the body must eliminate. Free radicals are produced by environmental sources (air pollution, chemicals, ionizing radiation, oxidized [rancid] fats, smoke and toxic heavy metals), immune system cells, the metabolism of oxygen, and numerous enzymatic reactions. Some free radical activity is required for normal physiological processes; these molecules are manufactured and secreted by white blood cells in order to destroy invaders such as fungi, microbes and virus. But in fending off infections, a surplus of free radicals are produced and released into surrounding tissue. Host cells can be damaged as well. A normal oxygen atom has four pairs of electrons. The body's natural metabolism can rob the atom of an electron which changes a normal healthy cell into a chemically-altered, damaged biological molecule - a free radical - which tries to replace the lost electron by raiding other molecules. When a free radical takes an electron from a cell wall, a new free radical is created, beginning a chain reaction. The electron theft erodes the cell membrane, leading to the disintegration/destruction of the cell. Thus the immune system and general health can be compromised by frequent infections and other sources of oxidative stress that introduce a cumulative and damaging abundance of free radicals. Each cell of the human body is equipped with a protective means of preventing or neutralizing these free radical reactions and repairing damage already caused by them. This protection is found in a diverse range of molecules referred to as antioxidants. A potent antioxidant system is manufactured by a cell in the form of enzymes: catalase, glutathione peroxidase and superoxide dismutase; endogenous molecules: alpha lipoic acid, bilirubin, coenzymeQ10, glutathione, sulfhydryl groups, thioredoxin and urate; exogenous molecules: bioflavonoids, mannitol, phenolic acid derivatives and proanthocyanidins; and essential nutrients: carotenoids, cysteine, selenium, and vitamins A, vitamin C and vitamin E. These molecules can neutralize toxic forms of oxygen (free radicals) or convert them into less dangerous products. Imbalance between free radical production and antioxidant defense can result in oxidative stress which can cause a depletion of these molecules, deactivation of some enzymes, activation of others (such as proteases), DNA strand breakage, or damage to cell membranes - allowing the leakage of substances that can generate additional damage. Some degree of oxidative stress occurs in most, if not all, human diseases. It is important to note that certain antioxidants become free radicals when they take on electrons from the free radicals they inactivate. Medical research shows that antioxidants taken individually do not provide a complete defense against free radicals, since no one antioxidant destroys all free radicals, but a variety of antioxidants taken together, commonly referred to as an antioxidant cocktail, are more effective in enhancing the body's defense against all free radicals. For example, after vitamins C and vitamin E destroy free radicals, their chemical structures change and they become free radicals (pro-oxidant), but other antioxidants such as alpha lipoic acid and glutathione, via enzymatic reactions in cells, recharge oxidized molecules such as vitamins C and vitamin E and recirculate them back into their original stabilized (antioxidant) state. In addition, when cells are exposed to nitrogen dioxide, uric acid seems to be a major protective antioxidant, whereas it appears to play little role as a scavenger of hypochlorous acid. Similarly, when cells are exposed to cigarette smoke, lipid peroxidation occurs which is inhibited by vitamin C, whereas vitamin C has no effect on the formation of protein carbonyls by cigarette smoke. As an extreme example, some known carcinogens that aggravate oxidative DNA damage in vivo are powerful inhibitors of in vitro lipid peroxidation. Thus, it is this synergistic interrelationship among antioxidants that supports the necessity for repletion with an antioxidant cocktail rather than repletion with an individual antioxidant, thereby providing the cells with constant protection from cellular damage due to excessive and varied free radical activity. Pharmaceutical drugs that can cause antioxidant deficiencies include acetohexamide, amitriptyline, amoxapine, aspirin, atorvastatin, benzthiazide, beta-blockers, bumetanide, cerivastatin, chlorothiazide, chlorpromazine, chlorpropamide, cholestyramine resin, choline magnesium trisalicylate, choline salicylate, clomipramine, clonidine, colchicine, colestipol, corticosteroids, desipramine, doxepin, ethacrynic acid, fluphenazine, fluvastatin, furosemide, glimepiride, glipizide, glyburide, haloperidol, hydralazine, hydrochlorothiazide, hydroflumethiazide, imipramine, indapamide, isoniazid, lovastatin, mesoridazine, methyclothiazide, methyldopa, metolazone, mineral oil, neomycin, nortriptyline, oral contraceptives, perphenazine, polythiazide, pravastatin, prochlorperazine, promazine, promethazine, protriptyline, quinethazone, simvastatin, thiethylperazine, thiroidazine, tolazamide, tolbutamide, torsemide, trichlormethiazide, trifluoperazine and trimipramine. > back to top |
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