Surgery: light – thermal – and electrical application – Light – thermal – and electrical application – Electrical therapeutic systems
Reexamination Certificate
2002-05-23
2004-06-15
Bockelman, Mark (Department: 3762)
Surgery: light, thermal, and electrical application
Light, thermal, and electrical application
Electrical therapeutic systems
C128S898000
Reexamination Certificate
active
06751506
ABSTRACT:
FIELD OF THE INVENTION
This invention pertains to a method for enhancing antioxidant levels in human beings without administration of exogenous antioxidants through diet or supplements.
BACKGROUND OF THE INVENTION
Oxidative stress is thought to be involved in the aging process in aerobic organisms and to play a role in the pathogenesis of several disease states, including Alzheimer's disease, myocardial infarction, atherosclerosis, Parkinson disease, autoimmune diseases, radiation injury, emphysema, sunburn, glomerular disorders, schizophrenia, sickle cell disease, leukemia, osteoporosis, infertility, cancer, retinopathy, and noise-related hearing impairment. Oxidative stress is the result of free radicals, such as the hydroxyl radical, reacting with biological macromolecules, such as lipids, proteins, nucleic acids and carbohydrates. The initial reaction generates a second radical, which in turn can react with a second macromolecule to continue the chain reaction. In the process of reacting, a free radical can modify protein or DNA structures, disrupt individual nucleotide bases, and thereby cause effects such as single-strand breaks and cross-linking in nucleic acids. Free radical-induced oxidative stress has been associated with a number of major cardiovascular disease risk factors. See “Reactive Oxygen Species (ROS)” (first printed in R & D Systems' 1997 Catalog), available at http://www.rndsystems.com/asp/g_sitebuilder.asp?bodyId=222.
A current theory holds that free radical-induced oxidative stress is a major factor in the long-term tissue degradation associated with aging. This free radical theory proposes that aging is the cumulative result of oxidative damage to the cells and tissues of the body that arises primarily as a result of aerobic metabolism. Several lines of evidence have been used to support this hypothesis including the claims that: (1) Variation in species life span is correlated with metabolic rate and protective antioxidant activity; (2) enhanced expression of antioxidative enzymes in experimental animals can produce a significant increase in longevity; (3) cellular levels of free radical damage increases with age; and (4) reduced calorie intake leads to a decline in the production of free radical and an increase in life span. The free radical theory may also be used to explain many of the structural features that develop with aging including the lipid peroxidation of membranes, formation of age pigments, cross-linkage of proteins, DNA damage and decline of mitochondrial function. Wickens, A. P., “Ageing and the free radical theory,” Respir. Physiol., Vol. 128(3), pp. 379-91 (2001).
Free radicals only occur in trace quantities in biological tissues and are extremely reactive. Because of the difficulty of directly measuring free radicals in vivo, measurements can be made using biomarkers, for example, an assay of antioxidant vitamins and free radical scavengers. Therefore, oxidative stress has been mainly observed through such indirect biomarkers of free radical-induced damage. In aerobic organisms, oxidative damages to tissues and organs is prevented by a network of defenses which include antioxidant and repairing enzymes, as well as small molecules with scavenging ability, such as antioxidant vitamins. For these reasons, the assay of antioxidant vitamins and of small molecular free radical scavengers in biological milieus may be used, if appropriately performed, to quantify the defense status against oxidative damage and to provide an indirect estimate of free radical production in aging humans. Polidori, M. C., et al., “Peripheral non-enzymatic antioxidant changes with human aging: a selective status report,” Biogerontology, Vol. 2(2), pp. 99-104 (2001).
Malondialdehyde (MDA) levels both in blood and urine have been one of the most widely used free radical markers. Measurement of MDA excretion in the urine became available in 1964. MDA is the end product of lipid peroxidation, and this urinary calorimetric assay represents by far the simplest approach to measurement of free radical activity. Furthermore, this colorimetric assay has been highly statistically significantly correlated with the fluorometric approach.
Mammalian cells possess elaborate defense mechanisms to detoxify radicals. Radical-scavenging antioxidants (e.g., vitamin E) interrupt the chain by capturing the radical; the vitamin E radical is relatively stable, and it can be enzymatically converted to its non-radical form. Excessive amounts of cellular oxidants, which animal cells constantly produce, can induce oxidative damage. Cellular antioxidants provide a defense against the damaging effects of the cellular oxidants. However, in moderate concentrations, cellular oxidants are necessary for a number of protective reactions which eliminate cancerous and other life-threatening cells, such as anti-microbial phagocytosis and apoptosis. Excess antioxidants could inhibit the protective anti-cancer function that the apoptosis process provides. Abundant antioxidants might suppress these protective functions, particularly in people with a low innate baseline level of cellular oxidants. Salganik, R. I., “The benefits and hazards of antioxidants: controlling apoptosis and other protective mechanisms in cancer patients and the human population,” J. Am. Coll. Nutr., Vol. 20(5 Suppl.), pp. 464S-472S (2001).
Conventional antioxidant supplements comprise, for example, vitamin C, vitamin E, beta-carotene, or other forms such as red ginseng or DHEAs, for example. Given that antioxidant supplements can actually be harmful in high doses to patients who have low levels of baseline cellular oxidants, safe antioxidant supplement use requires an accurate dosage level corresponding to each patient's needs. Each patient's baseline needs would have to be determined periodically because it is also clear that the optimal dosage of antioxidant supplements probably varies over time with each patient. Meagher, E., et al., “Antioxidant therapy and atherosclerosis: animal and human studies,” Trends Cardiovasc. Med., Vol. 11 (3-4), pp. 162-5 (2001).
In healthy individuals, a delicate balance exists between the production of free radicals and the production of antioxidants. Free radicals are produced in the body as byproducts of normal metabolism and as a result of exposure to radiation and some environmental pollutants. They are normally neutralized by the body's production of antioxidant enzymes (super oxide dismutase, catalase, and glutathione peroxidase) and the nutrient-derived antioxidant small molecules (Vitamin E, Vitamin C, carotene, flavonoids, glutathione, uric acid, and taurine). In some pathological conditions, the natural balance can be upset by oxidative stress in the presence of certain diseases, such as diabetes. The oxidative stress can cause a reduction in the body's normal production of antioxidants. To prevent deterioration of antioxidant levels, it is conventionally recommended to consume adequate amounts of antioxidant-rich foods, e.g., fruits and vegetables, and also to take supplements as necessary. Sardesai, V. M., “Role of antioxidants in health maintenance,” Nutr. of Clin. Pract., Vol. 10(1), pp. 19-25 (1995).
Despite the extensive research in the use of antioxidants, there is not a clear-cut consensus that these antioxidants are totally successful in reducing free radicals. Sacheck, J. M., et al., “Role of Vitamin E and Oxidative Stress in Exercise,”
Nutrition
, Vol. 27(10), pp. 809-14 (2001), Meagher, E., et al., “Antioxidant Therapy and Atherosclerosis: Animal and Human Studies,”
Trends Cardiovasc. Med
., Vol. 11(3-4), pp. 162-5 (2001). Although cancer tissue has significant decreases in glutathione, vitamin C, and vitamin E, there is no evidence that taking the supplements actually prevents cancer. Skrzydlewska, E., et al., “Antioxidant Status and Lipid Peroxidation in Colorectal Cancer,”
Toxicol. Environ. Health A
., Vol. 64(3), pp. 213-22 (2001). On the other hand, there is considerable evidence that the antioxidants found in natural sources
Bockelman Mark
Foley & Lardner
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