Vitamin C is itself not a sunscreen. Topical vitamin C protects against solar damage primarily as an antioxidant which deactivates the UV-induced free radicals, most significantly the superoxide anion, singlet oxygen, and the hydroxyl radical. Vitamin C is equally effective in protecting against both UVB (290-320 nm) and UVA (620-400 nm) (4). On both porcine and human skin, applying vitamin C decreases the acute erythema and sunburn suffered even when applied after sun exposure (4). Protection is confirmed by histologic examination. Treatment of porcine skin in vivo with topical 10% vitamin C decreases the number of abnormal apoptotic “sunburn cells” by 40% to 60% (4) and reduces the UV damage to DNA by 62% (4).
Topical vitamin C further prevents UV-induced immonosuppression (5). In approximately one-third of humans, the activity of the immune system is inhibited after exposure to sunlight. This immunosuppression is measured by the class of contact hypersensitivity to sensitizers such as poison ivy. Sunscreens only partially aid in the prevention of UV immunosuppression. Animal studies demonstrate that topical vitamin C prevents this UV-induced loss of contact hypersensitivity as well as UVB – induced tolerance.
Topical vitamin C is also directly anti-inflammatory (further accounting for decreased erythema after sun exposure). Laser resurfacing causes redness for at least three to four months. With vitamin C applied before and after laser resurfacing surgery, redness is decreased after only two months (6). Dermatologic surgeons recommend using topical vitamin C as long as possible prior to laser resurfacing and beginning again as early as fourteen days following surgery. Topical vitamin C can also be used effectively to treat the inflammation of rosacea (7).
The main action of vitamin C on the skin is direct stimulation of collagen synthesis. Vitamin C is an essential cofactor for the two enzymes required for collagen synthesis, prolyl hydroxylase (which makes the collagen molecule stable) and lysyl hydroxylase (which cross-links the collagen to give structural strength) (8). Recent research has further demonstrated that vitamin C acts directly on DNA to increase the transcription rate and to stabilize the pro-collagen messenger RNA, thus regulating and maintaining the intercellular amount of collagen (9).
Exciting experiments have demonstrated that vitamin C also has anti-aging effects. Studies in vitro compared newborn with elderly (80-95 year-old) fibroblasts (10). Elderly cells proliferate in vitro at only one-fifth of the rate of newborn cells. However, when vitamin C is added to the culture medium, the elderly cells actually proliferate better than normal newborn fibroblasts. Even the newborn fibroblasts proliferate almost four times better when exposed to vitamin C (10).
Not only do fibroblasts increase proliferation in the presence of vitamin C, but they also synthesize more collagen. Newborn fbroblasts synthesize a larger percentage of collagen than elderly cells, but again, when elderly cells are exposed to vitamin C in vitro,
they produce more collagen than the normal, newborn fibroblasts (10). Surprisingly, also the newborn cells double the amount of collagen synthesized (10).
Vitamin C further reverses the adverse appearance of photoaging by inhibiting tyrosinase (11), thereby fading unattractive solar lentigos. Because L-ascorbic acid may inhibit elastin biosynthesis (12), it may reduce the solar elastosis of photoaged skin.
Another important action of vitamin C on the skin is that topical vitamin C actually increases the synthesis of several very specific lipids of the skin surface (13). Not only does this mean that vitamin C helps the natural moisturization of the skin, but it also enhances the protective barrier function of the skin (14).