Sunscreens may also contain substances that help protect our skin from other unseen damage from the sun. This section discusses these substances, known as cell protectants.
Background: How Cell Protectants Work
UVA radiation penetrates deeply into our skin and initiates oxidation processes at the cellular level. Exposure to UVA causes pigmentation changes such as tanning or burning. A variety of cell-damaging free-radical oxygen species, including superoxide (*O2), and hydroxy radicals (*OH) are released vis-à-vis UVA induction. Cellular damage then occurs, particularly by membrane lipids’ peroxidation. Hydrogen peroxide may also form, adding to cellular damage. The primary action of UVA is to add energy to molecules in our skin, including ubiquinone (Coenzyme Q10), that go on to interact with oxygen to produce the highly reactive oxygen forms mentioned above. These “oxygen” moieties degrade DNA in our cells.
Evidence of UVA damage becomes visible first as sunburn (where it adds to UVB burning), then inflammation and skin darkening, and later as photoaging and skin cancers. The Skin Cancer Foundation has reported that depletion of Vitamin A in the skin by UVA exposure may contribute to both photoaging and cancers of the skin.
Active and Supportive Cellular Protection
Protecting the skin from the adverse effects of UVB and UVA is the first line of defense. For UVB, adequate concentrations of approved “sunscreens” will achieve a protection factor (SPF) of 30 – plus. Several chemical absorbers will give moderate (not adequate) protection against the lower-half of the UVA spectrum (315nm – 350/360nm). The most recently approved UVA absorbing chemical, Parsol 1789 â (avobenzone), gives good protection through a greater portion of the UVA region (up to approximately 370nm – 374nm), but is still incomplete and believed to be photo-unstable. Additionally, avobenzone is reported to be photo-unstable, rapidly degrading on exposure to UV radiation. Of equal or greater concern are reports indicating that UVB sunscreens may be degraded by an avobenzone – photo-sensitized mechanism. In other words, avobenzone appears to not only rapidly lose its UVA photoprotecting ability, but may actually decrease the protection level of UVB sunscreens. These reports urge very careful formulating and thorough testing, as well as adding stabilizer molecules when/if incorporating avobenzone into a UV protecting product.
To increase protection against UVB and UVA cellular damage, physical blockers, including iron oxides, titanium dioxide and zinc oxide, as well as extenders (particles that extend the effectiveness of the smaller particles of physical blockers) such as mica and talcum must be included. Of primary importance is that these physical protectants be incorporated at adequate concentration to afford complete protection for extended periods.
Supplementary cellular protectants are not intended to act as primary UV absorbers (though some may exhibit slight absorption within the UVB – UVA spectrum). Rather, they act to prevent damage to the cells directly and indirectly.
A partial list of examples of common cellular protectants used in sunscreen follows. This is not an all inclusive list; but rather, a review of cell protectants with different modes or sites of active protection.
In its pure active “natural “ state, as tocopherol, vitamin E protects products from oxidizing, but is too reactive to retain adequate activity within the skin when topically applied. Fortunately, our skin can metabolize more stable forms of vitamin E to release tocopherol where it is needed. Tocopheryl acetate and tocopheryl linoleate are among the more popular forms used in sunscreens. As an oil-soluble antioxidant, it gives considerable protection to our skins’ cells. Vitamin E “breaks” the chain-reaction of free- radicals before they can cause lipid peroxidation-induced destruction of the cellular membranes. However, it requires a regeneration agent, a substance that prevents it from being rapidly depleted. Vitamin C (see below) is one such regeneration agent.
Human beings do not produce vitamin C themselves. We rely entirely on the vitamin C we get from our diets. Vitamin C is normally deposited in the skin and is an essential part of the anti-oxidant brigade to protect skin against free radical assault from UV light.
Vitamin C (ascorbic acid) is one of the most effective antioxidants available and is used in sunscreen to regenerate the lipid-soluble vitamin E (so that it retains its cellular membrane protective activity). Vitamin C is available in many forms, some of which are water-soluble (ascorbyl acid phosphate, for example), while others are lipid-soluble, such as ascorbyl palmitate. Ascorbyl palmitate, topically applied, has also been reported to exhibit some protection against UVB burns and has anti-inflammatory activity. Combinations of vitamin C compounds with vitamin E appear to offer greater protection against cellular insult from UVB and/or UVA exposure than either antioxidant alone. Additionally, Vitamin C moderately protects against UVB photodamage as well as UVA-promoted phototoxic responses.
Normally found in the skin as retinyl palmitate, Vitamin A is the dominant vitamin of the skin because it has a fundamental role in the control of normal activities of skin cells. It also is of great importance in controlling normal activities of the DNA of the nucleus of the cell as well as the mitocondria. Vitamin A is extremely sensitive to sunlight and particularly to UVA (315-400nm) light.
This pre-cursor of vitamin A, a lipid-soluble (i.e. oil soluble) yellow–orange/orange-red pigment, is found in most vegetables. Beta-Carotene is an excellent quencher of singlet oxygen (free radical) as well as free radicals that participate in lipid peroxidation. B-Carotene has been reported to be of value in the treatment of erythropoietic protoporphyria (EPP), a disease that causes photosensitivity to upper UVA and sections of visible light (380nm – 560nm). Additionally, there is evidence that Beta-Carotene inhibits UV’s promoted carcinogenesis.
These bioflavanoid-like antioxidants are found in vegetation such as pine bark (The Maritime Pine yields a highly active proanthocyanidin, offered under the trademark
Pycnogenol) and grapes. These compounds are among the most active free-radical quenchers known. Anthocyanins increase the action of ascorbates (Vitamin C) and supplement the protective qualities of tocopherol (Vitamin E). Published reports describe the ability of these highly specialized antioxidant bioflavanoids to not only potentiate vitamin C, protect cells and collagen tissue, but to strengthen blood vessels and maintain capillaries.
Numerous medical, pharmaceutical and nutritional publications describe the ability of selenium, in very low doses, to help prevent cancer, including skin cancer, act as an anti inflammatory, and aid in cellular DNA repair. It has also been reported that selenium reduces the reactivity of skin cells to UV exposure. Complex selenium compounds, topically applied in concentrations of less than 0.05% (selenium), significantly reduce UV skin damage (manifested as less inflammation, less pigmentation, and retardation of and diminished levels of skin cancer).
Chelates are compounds that bind metals, particularly iron, and remove them from interacting with other materials. Some chelates are formed naturally, others are synthesized. Iron chelators protect against cellular damage from free-radical(s) oxygen. A few chelating compounds are ortho-phenanthroline, edetic acid (and its salts/derivatives) and dipyridylamine. Topical chelate application prior to UV exposure is reported to reduce and/or delay visible skin wrinkling caused by UV exposure, as well as tumor formation.
Miscellaneous Photoprotective /Cell Aids
Some materials indirectly protect the skin cells from light wave damage by either maintaining the UV absorbers on the skin surface, such as octyldodecyl neopentanoate, or by forming a maze (matrix)– like film that tightly bonds to the skin surface. These materials, such as acrylates/octylpropenamide copolymer and aluminum starch octenylsuccinate, significantly lengthen the pathway of light trying to reach to skin, thereby reducing the light’s ability to damage skin cells.