Drug – bio-affecting and body treating compositions – Designated organic active ingredient containing – C-o-group doai
Reexamination Certificate
2000-04-13
2002-08-13
Henley, III, Raymond (Department: 1614)
Drug, bio-affecting and body treating compositions
Designated organic active ingredient containing
C-o-group doai
C514S724000, C514S691000, C424S400000, C424S401000, C424S059000
Reexamination Certificate
active
06433025
ABSTRACT:
FIELD OF THE INVENTION
This invention relates to the treatment and prevention of sunburns by UV light exposure. More particularly the invention relates to a method for prevention of sunburns using, as a basis, the protective properties of astaxanthin. Most particularly, the invention relates to prevention of sunburns using orally administered astaxanthin.
BACKGROUND OF THE INVENTION
Tanning is pigmentation of the skin due to the synthesis and dispersion of melanin in the epidermis. It is of great cosmetic and societal significance and a key physiological defense against sun-induced injuries such as sunburn, photocarcinogenesis and photoaging. However, during recent decades, there has been a dramatic increase in skin cancers, including melanoma, due to habitual sun exposure. At present, in the United States, about one in 75 individuals are projected to develop malignant melanoma during their lifetime. Unfortunately, progress in preventing sun-related injuries has been slow, in part due to lack of understanding of the molecular mechanisms involved in pigmentation.
There have been increasing incidence and mortality rates due to melanoma in most countries where they are being recorded. The highest incidences occur in areas with the highest flux of solar radiation such as the southern US, regions near the equator or at higher elevations. Ultraviolet radiation (UVR) increases about 4% for every 1000 feet in elevation. Lighter-skinned individuals are affected more frequently and severely. Significant transmission of UVR may occur through some types of clothing resulting in sunburned skin. The initial approach in many countries has been to develop some form of early detection program in an attempt to diagnose and treat at a curable stage the melanomas that are occurring now. The long-term morbidity and mortality associated with chronic sun exposure is related primarily to the development of cutaneous neoplasms, including basal cell carcinoma and malignant carcinoma.
Primary prevention of melanoma is a more long-term approach to the problem which many countries are now considering and a number are actively pursuing. A survey conducted at Galveston beach showed that the likelihood of sunburn increased with increasing duration of sun exposure, with 100% of subjects experiencing sunburn after 4.5 hours of exposure. Men exhibited a significantly higher frequency of sunburn, employed fewer sun-protective measures, and demonstrated less knowledge concerning sun safety information and skin cancer than women. The information suggests a need for greater educational efforts directed toward changing public attitudes about preventing sunburn, especially those of men, that currently lead to high-risk sunbathing behavior (McCarthy et al. 1999).
Sunburns are an acute inflammation reaction of the skin and tissue just beneath it that follows excessive exposure of the skin to UVR. The affected area becomes red, hot, tender, and swollen and in severe cases blisters may form. The ultraviolet spectrum can be divided in UVA (320-400 nm), UVB (290-320 nm) and UVC (200-290 nm), wavelengths less than 290 nm are filtered out in the outer atmosphere and are not encountered at sea level. About 65% of the total UVR reaches the earth between 10 AM and 2 PM. UVB radiation are high intensity rays absorbed by the surface of the skin and the primary cause of sunburns, erythema and intermediate skin damage. UVA rays are lower intensity but penetrate below the skin surface causing long-term damage such as premature wrinkling. UVA comprises the majority of the total UVR reaching the surface of the earth (about 90% at midday) and accounts for a significant percentage of the acute and chronic cutaneous effects. UVC and UVB produce damage primarily by the formation of cyclobutane pyrimidine dimers of DNA. Pyrimidine dimers are 80-90% of the UV-light induced DNA photoproducts, with the remainder being pyrimidine (6,4) pyrimidone (Franklin and Haseltine, 1986).
Recent concern about stratospheric ozone depletion has contributed to the desire for the primary prevention approach. There are epidemiological data associating the risk of melanoma with increased exposure to sunlight in people with fair skin. The exact spectrum of radiation in sunlight which is responsible for these tumors is not known, although the ultraviolet range is believed to be most important, particularly UVB but probably also UVA. Studies show that sunburns in childhood result in increased risk of melanoma later in life. Protecting children is especially important since more than half of a person exposure occurs before the age of 20. It is estimated that approximately 80% of the skin changes commonly thought of as skin aging (premature wrinkles, leathery skin, 30 freckles, dark spots) are actually due to sun exposure and not to the actual age of the skin. The aging process affects the skin's ability to protect itself. The rate of cell protection and turnover slows down with age, making cell repair less effective. The outer layer epidermis of the skin becomes thinner and melanocytes gradually lose their pigment producing ability, thereby reducing protection for the skin.
Skin cancer is the most common type of cancer, about 800,000 cases occur in the US each year. Most skin cancers are either basal cell or squamous type and tend to grow and spread slowly. Nearly 95% can be cured. Malignant melanoma is a much more serious form of skin cancer and is now increasing by about 4% per year. Melanoma was diagnosed in approximately 38,300 Americans in 1996. The overall five-year survival rate for melanoma is 85%. The five-year survival rate for localized disease is 93% and about 82% of melanomas are diagnosed in this earlier stage. The second-most common form of skin cancer, squamous cell carcinoma, appears as nodules or red scaly patches, and can spread if untreated. While the cure rate is relatively high, squamous cell carcinoma results in at least 1,200 deaths per year (Park and Gilchrest. 1999).
Less intense or shorter-duration exposure to UVR results in an increase in skin pigmentation that provides some protection against further UVR-induced damage. The increased skin pigmentation occurs in two phases, immediate pigment darkening and delayed tanning. Intermediate pigment darkening occurs during exposure to UVR and results from oxidation and redistribution of existing melanin. This reaction may fade rapidly or persist for several days. Delayed tanning results from increased synthesis of epidermal melanin and requires 24-72 hours to become visible. With repeated exposure to UVR, the skin thickens due to epidermal hyperplasia and thickening of the stratum corneum.
The minimal single dose of UVR (energy per unit area) required to produce erythema on exposed skin is known as minimal erythema dose (MED). Moderate to severe sunburn occurs at 3-8 MED's. UVR penetrates moist skin more effectively than dry skin. MED's are greater on the limbs than on the face, neck and trunk. Exposure to solar radiation has beneficial benefits of stimulating cutaneous synthesis of vitamin D. However, when skin is subjected to excessive radiation in the ultraviolet range (less than 400 nm), deleterious effects such as sunburn or ‘solar erythema’ can occur. Solar erythema is associated with microscopic changes in the skin that are detectable within 30 minutes of UVR exposure. The most characteristic changes include formation of epidermal sunburn cells, damaged keratinocytes with hyaline cytoplasm and pyknotic nuclei. Epidermal Langerhans cells and mast cells may decrease while the relative percentage of hypogranulated or degranulated cells may increase. Superficial blood vessels show endothelial swelling, perivenular edema and a mixed perivascular infiltrate. The precise biochemical pathways that lead to the sunburn reaction are not fully understood, but appear to involve multiple mediators including histamine, prostaglandins and cytokines. Sunburns may cause exacerbation of other skin diseases, and trigger recurrence of herpes simplex, lupus, porphyria or other cutaneous disor
Cyanotech Corporation
Devine, Millimet & Branch P.A.
Henley III Raymond
Jagoe Donna
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