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[Important Facts about N-Acetyl Cysteine | The N-Acetyl Cysteine to Glutathione Conversion] [Benefits of High Glutathionine Levels | references]
N-acetyl cysteine is a powerful antioxidant. Antioxidants neutralize free radicals, the toxic waste products of cellular metabolism. If free radicals are left unchecked, they damage cells, and are considered by many scientists to be major factors in the aging process. N-acetyl cysteine has also been shown to give powerful protection against a broad range of toxic hazards. These include acrolein (found in barbecue and cigarette smoke, and auto exhaust), bromobenzene, paraquat (a toxic herbicide), overdoses of acetaminophen, and the side effects of both cyclophosphamide and adriamycin (anti-cancer drugs), and halothane (an anesthetic). The key to this protection may be the sulfur and sulfhydryl groups contained in both N-acetyl cysteine and its derivative, glutathione. The N-Acetyl Cysteine to Glutathione Conversion Although the protection it offers is extremely important, an equally vital role is N-acetyl cysteine's conversion to glutathione, another compound with powerful detoxifying abilities. Glutathione is an amino acid compound made of glycine, L-glutamic acid and L-cysteine. Since the first two are plentiful in our diets, the amount of glutathione our bodies can produce is limited by the amount of cysteine, and this is sometimes in short supply. This is why cysteine is called the rate limiting factor in the production of glutathione. Although cysteine or methionine are good glutathione precursors, N-acetyl cysteine is by far the best. L-cysteine loses approximately 85% of its sulfur groups (which become the active part of glutathione) in the digestion process. N-acetyl cysteine may have an anti-aging effect by increasing glutathione Ievels, particularly in the liver, lungs, kidneys, and bone marrow, which use both compounds for protection. An early 1970's experiment demonstrated N-acetyl cysteine’s superior protective abilities. Acetaldehyde is a toxic by-product of cigarette smoke, alcohol and Candida albicans. In a series of trials testing the protective effects of many nutrients on acetaldehyde toxicity, Herbert Sprince, M.D., showed that supplemental N-acetyl cysteine is more bioavailable and effective than supplemental glutathione or L-cysteine. Science Shows Benefits of High Glutathione Levels
Experiments indicate that intracellular glutathione levels affect the ability of lung phagocytes (a type of white blood cell which ingests and destroys bacteria, cellular debris, dust particles, etc.) to do their job. In a classic experiment reported in Science in 1968, Gareth Green of Harvard Medical School demonstrated that cigarette smoke seriously reduced the ability of phagocytes to destroy bacteria. When glutathione was added to the poisoned phagocytes, their loss of effectiveness was completely reversed. Glutathione is also a major part of two key antioxidant enzymes, glutathione-S-transferase and glutathione peroxidase. Glutathione-S-tranferase is a broad-spectrum liver-detoxifying enzyme. Glutathione peroxidase is one of the body's three main antioxidant enzyme systems, and is responsible for blocking cellular damage from free radicals, such as rancid fats. Glurathione peroxidase's protective ability has truly far-reaching implications. Rancid fats can suppress an enzyme called prostacyclin synthetase, which generates prostacyclin. Prostacyclin is the most important of the hormone-like prostaglandins for protecting artery linings. A powerful antidote to our polluted environment, supplementing your diet with N-Acetyl Cysteine is a simple, yet profound way to protect yourself.
L Borgstrom,et.al., European Journal of Clinical Pharmacology (1986) 31: 217-122. L. Bonahoni & A. Gazzainga, European Journal of Respiratory Disease (1980) 61, Supplement 111, 45-51. H. Sprince, et. al., Agents and Actions (1975) 5: 164-173. L. Levine & P Kidd, Antioxidant adaptation: Its Role in Free Radical Pathology Second Edition (1986) Biocurrents Press, San Francisco. G.M. Green, Science (1968) 162: 180-811. M.H. Luria, Medical Hypotheses (1990) 32: 21-28. J.R. Dawson, et. al., Archives of Toxicology (1984) 55: 11-15. A. Lorber, et. al., Journal of Clinical Pharmacology (1973) 13: 332-336.
©1997 Source Naturals, Inc. Reprinted with exclusive permission from Source Naturals, Inc. |
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