Free radicals, in particular oxygen radicals, in mammalian cells arise from a variety of environmental sources. Such sources include smoke, pollution including ozone and radiation in addition to normal cell metabolism and inflammatory processes. Free radicals are known to be damaging to biological tissue components such as structural proteins, membrane lipids and nucleic acids, resulting in alteration or loss of tissue and cell function, cell death, and cancer. A well recognized source for generation of tissue damaging radicals is radiation, such as UV radiation which causes high levels of radical production in the skin, leading to skin cancer and pre-mature skin aging (skin wrinkling). The use of tocopherol sorbate for preventing ultraviolet-induced damage to skin is disclosed in U.S. Pat. No. 4,847,072 issued to Bissett and Bush on Jul. 11, 1989.
Based on a growing body of evidence, it is believed that free radicals produced as by-products in normal metabolism can cause damage which is responsible for chronological aging of all tissues, including the skin. This has been termed the free radical theory of aging. Such free radicals are often produced by causes other than exposure of tissues to ultraviolet light. Free radicals produced by normal metabolism can cause skin damage, via protein oxidation (also known as glycation) and inflammation.
Nonultraviolet induced free radicals can also cause pigmentation of the skin. This can include post-inflammatory hyperpigmentation that results from acne, insect/spider bites, allergic reactions, irritation from topical materials, drug phototoxicity (from oral or topical drug dosing), infections of bacterial or fungal nature, recovery from injuries such as cuts or blisters, razor bumps (especially from in-grown hairs), and the like.
The mammalian body has a variety of anti-radical defenses, such as small molecule anti-oxidants (e.g., vitamin C, vitamin E, beta-carotene) and anti-oxidant enzymes (e.g., superoxide dismutase, catalase). However, these defenses are often not sufficient to combat the levels or types of radicals produced from environmental or endogenous sources. Therefore, to more completely combat the damaging effects of free radicals, especially oxygen radicals, free radical scavengers and anti-oxidants can be used. These compounds react with the radical species to convert them to stable, non-reactive materials.
It is an object of the present invention to provide methods for reducing nonultraviolet-induced free radical damage in mammalian cells.
It is a further object of the present invention to provide methods for preventing or treating pollution-based skin damage to provide benefits of skin texture protection, barrier protection, prevention of skin sensitivity and prevention of skin dryness.
It is a futher object of the present invention to provide methods for preventing or treating metabolism-induced skin damage to provide benefits of preventing chronological skin aging changes (sagging, sallowness), preventing thinning of the skin (atrophy), and preventing loss of functional blood vessels.
It is a further object of the present invention to provide methods for preventing or treating free radical-induced pigmentation of the skin.
It is a further object of the present invention to provide skin care compositions which can be used to carry out the foregoing methods.